Gene Summary

Gene:PECAM1; platelet and endothelial cell adhesion molecule 1
Aliases: CD31, PECA1, GPIIA', PECAM-1, endoCAM, CD31/EndoCAM
Summary:The protein encoded by this gene is found on the surface of platelets, monocytes, neutrophils, and some types of T-cells, and makes up a large portion of endothelial cell intercellular junctions. The encoded protein is a member of the immunoglobulin superfamily and is likely involved in leukocyte migration, angiogenesis, and integrin activation. [provided by RefSeq, May 2010]
Databases:OMIM, HGNC, Ensembl, GeneCard, Gene
Protein:platelet endothelial cell adhesion molecule
Source:NCBIAccessed: 30 August, 2019


What does this gene/protein do?
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Pathways:What pathways are this gene/protein implicaed in?
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Cancer Overview

Research Indicators

Publications Per Year (1994-2019)
Graph generated 30 August 2019 using data from PubMed using criteria.

Literature Analysis

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Tag cloud generated 30 August, 2019 using data from PubMed, MeSH and CancerIndex

Latest Publications: PECAM1 (cancer-related)

Wang HF, Wang SS, Zheng M, et al.
Hypoxia promotes vasculogenic mimicry formation by vascular endothelial growth factor A mediating epithelial-mesenchymal transition in salivary adenoid cystic carcinoma.
Cell Prolif. 2019; 52(3):e12600 [PubMed] Related Publications
OBJECTIVES: To investigate the role of hypoxia in vasculogenic mimicry (VM) of salivary adenoid cystic carcinoma (SACC) and the underlying mechanism involved.
MATERIALS AND METHODS: Firstly, wound healing, transwell invasion, immunofluorescence and tube formation assays were performed to measure the effect of hypoxia on migration, invasion, EMT and VM of SACC cells, respectively. Then, immunofluorescence and RT-PCR were used to detect the effect of hypoxia on VE-cadherin and VEGFA expression. And pro-vasculogenic mimicry effect of VEGFA was investigated by confocal laser scanning microscopy and Western blot. Moreover, the levels of E-cadherin, N-cadherin, Vimentin, CD44 and ALDH1 were determined by Western blot and immunofluorescence in SACC cells treated by exogenous VEGFA or bevacizumab. Finally, CD31/ PAS staining was performed to observe VM and immunohistochemistry was used to determine the levels of VEGFA and HIF-1α in 95 SACC patients. The relationships between VM and clinicopathological variables, VEGFA or HIF-1α level were analysed.
RESULTS: Hypoxia promoted cell migration, invasion, EMT and VM formation, and enhanced VE-cadherin and VEGFA expression in SACC cells. Further, exogenous VEGFA markedly increased the levels of N-cadherin, Vimentin, CD44 and ALDH1, and inhibited the expression of E-cadherin, while the VEGFA inhibitor reversed these changes. In addition, VM channels existed in 25 of 95 SACC samples, and there was a strong positive correlation between VM and clinic stage, distant metastases, VEGFA and HIF-1α expression.
CONCLUSIONS: VEGFA played an important role in hypoxia-induced VM through regulating EMT and stemness, which may eventually fuel the migration and invasion of SACC.

Sandberg TP, Stuart MPME, Oosting J, et al.
Increased expression of cancer-associated fibroblast markers at the invasive front and its association with tumor-stroma ratio in colorectal cancer.
BMC Cancer. 2019; 19(1):284 [PubMed] Free Access to Full Article Related Publications
BACKGROUND: The tumor microenvironment has a critical role in regulating cancer cell behavior. Tumors with high stromal content are associated with poor patient outcome. The tumor-stroma ratio (TSR) identifies colorectal cancers (CRC) with poor patient prognosis based on hematoxylin & eosin stained sections. The desmoplastic reaction consists to a great extent of cancer-associated fibroblasts (CAFs) of which different subtypes are known. The aim of this study is to investigate and quantify CAFs present in the tumor stroma of CRC stratified by the TSR to possibly add prognostic significance to the TSR.
METHODS: The expression of established CAF markers was compared between stroma-low and stroma-high tumors using transcriptomic data of 71 stage I - III CRC. Based on literature, fibroblast and stromal markers were selected to perform multiplex immunofluorescent staining on formalin fixed, paraffin-embedded tumor sections of patients diagnosed with stage III colon cancer. Antibodies against the following markers were used: αSMA, PDGFR -β, FAP, FSP1 and the stromal markers CD45 and CD31 as reference. The markers were subsequently quantified in the stroma using the Vectra imaging microscope.
RESULTS: The transcriptomic data showed that all CAF markers except one were higher expressed in stroma-high compared to stroma-low tumors. Histologically, stroma-high tumors showed a decreased number of FSP1
CONCLUSIONS: The increased expression of FAP at the invasive part and in stroma-high tumors might contribute to the invasive behavior of cancer cells. Future functional experiments should investigate the contribution of FAP to cancer cell invasion. Combining the quantity of the stroma as defined by the TSR with the activity level of CAFs using the expression of FAP may result in an expanded stroma-based tool for patient stratification.

Li YJ, Qing X, Tao QX, et al.
Vasculogenic Mimicry Formation Is Associated with Erythropoietin Expression but Not with Erythropoietin Receptor Expression in Cervical Squamous Cell Carcinoma.
Biomed Res Int. 2019; 2019:1934195 [PubMed] Free Access to Full Article Related Publications
Background: Vasculogenic mimicry (VM), as an endothelium-independent cancer microcirculation, has been observed in many malignancies including cervical cancer. Erythropoietin (EPO) and erythropoietin receptor (EPO-R) could produce an angiogenic effect to promote cervical squamous cell carcinoma (CSCC) progression. However, the association between VM formation and EPO/EPO-R expression in CSCC is poorly explored.
Methods: Seventy-six paraffin-embedded CSCC samples, 25 high-grade squamous intraepithelial lesion (HSIL) samples, 20 low-grade squamous intraepithelial lesion (LSIL) samples, and 20 normal cervix samples were collected. Immunohistochemistry SP method was performed to detect EPO/EPO-R expression and CD31/periodic acid-Schiff (PAS) double staining was performed to detect VM formation. The associations of EPO/EPO-R and VM with clinicopathological parameters of CSCC were analyzed. The associations between VM formation and EPO/EPO-R expression were also analyzed.
Results: The positive expression rates of EPO and EPO-R were gradually increasing along the progression of normal cervix-LSIL-HSIL-CSCC sequence (
Conclusion: These data suggest that increased EPO/EPO-R expression may play an important role in cervical carcinogenesis. EPO overexpression may promote VM formation in CSCC.

Bekes I, Löb S, Holzheu I, et al.
Nectin-2 in ovarian cancer: How is it expressed and what might be its functional role?
Cancer Sci. 2019; 110(6):1872-1882 [PubMed] Free Access to Full Article Related Publications
Nectin-2 is an adhesion molecule that has been reported to play a role in tumor growth, metastasis and tumor angiogenesis. Herein, we investigated Nectin-2 in ovarian cancer patients and in cell culture. Tumor as well as peritoneal biopsies of 60 ovarian cancer patients and 22 controls were dual stained for Nectin-2 and CD31 using immunohistochemistry. Gene expression of Nectin-2 was quantified by real-time PCR and differences analyzed in relation to various tumor characteristics. In the serum of patients, vascular endothelial growth factor (VEGF) was quantified by ELISA. Effect of VEGF on Nectin-2 expression as well as permeability was investigated in HUVEC. In tumor biopsies, Nectin-2 protein was mainly localized in tumor cells, whereas in peritoneal biopsies, clear colocalization was found in the vasculature. T3 patients had a significantly higher percentage of positive lymph nodes and this correlated with survival. Nectin-2 was significantly upregulated in tumor biopsies in patients with lymph node metastasis and with residual tumor >1 cm after surgery. Nectin-2 expression was significantly suppressed in the peritoneal endothelium of patients associated with significantly increased VEGF serum levels. In cell culture, VEGF stimulation led to a significant downregulation of Nectin-2 which was reversed by VEGF-inhibition. In addition, Nectin-2 knockdown in endothelial cells was associated with significantly increased endothelial permeability. Nectin-2 expression in ovarian cancer may support tumor cell adhesion, leading to growth and lymph node metastasis. In addition, VEGF-induced Nectin-2 suppression in peritoneal endothelium may support an increase in vascular permeability leading to ascites production.

Rask L, Høgdall CK, Kjaer SK, et al.
Association of CD31 and p53 With Survival of Ovarian Cancer Patients.
Anticancer Res. 2019; 39(2):567-576 [PubMed] Related Publications
BACKGROUND/AIM: New markers for ovarian cancer are needed. This study aimed to examine the expression of tumour cell p53 and endothelial cell CD31 proteins and correlate them to clinicopathological factors.
PATIENTS AND METHODS: Expression of proteins was immunohistochemically assessed using tissue sections from 585-599 ovarian cancer patients from the Danish MALOVA study.
RESULTS: High CD31 expression was found in poorly differentiated tumours (p=0.0006), and high p53 expression was found in poorly differentiated cancers (p<0.0001), high clinical stage (p<0.0001), non-radical surgery (p<0.0001) and high serum CA-125 values (p<0.0001). CD31 expression showed no prognostic survival value, but high hazard ratios were found for patients with high p53 expression (HR=2.313, p<0.0001). An interaction was found between p53 and stage of cancer, suggesting a prognostic impact of p53 in low-stage, but not in advanced-stage cancer.
CONCLUSION: More than 5% of p53 tissue expression may predict shorter survival of ovarian cancer patients and may be useful for predicting the risk of disease progression in low-stage patients following primary surgery. CD31 has no strong prognostic value.

Song EJ, Ashcraft KA, Lowery CD, et al.
Investigating a chimeric anti-mouse PDGFRα antibody as a radiosensitizer in primary mouse sarcomas.
EBioMedicine. 2019; 40:224-230 [PubMed] Free Access to Full Article Related Publications
BACKGROUND: Olaratumab (LY3012207/IMC-3G3/Lartruvo™) is a fully human monoclonal antibody specific for platelet-derived growth factor receptor alpha (PDGFRα). Phase Ib/II trial results of olaratumab plus doxorubicin in adult patients with advanced soft tissue sarcoma (STS) supported accelerated FDA approval of this regimen. Radiation therapy (RT) is frequently used for high-risk localized STS. However, olaratumab has not been tested with concurrent RT. Here, we evaluate the chimeric anti-mouse PDGFRα antibody 1E10Fc as a radiosensitizer in a primary mouse model of STS.
METHODS: Primary STS were initiated in mice. When tumors reached 70 mm
FINDINGS: RT significantly delayed time to tumor quintupling compared to no RT (p < 0·0001) [two-way ANOVA], but no difference in tumor growth was seen between mice receiving isotype or 1E10Fc treatment regardless of concurrent RT. Lower microvessel density was observed in the 1E10Fc + RT group. Fewer mice treated with 1E10Fc had micrometastases, but this difference was not statistically significant (p < 0·09).
INTERPRETATION: 1E10Fc did not act as a radiosensitizer in this primary STS model.
FUNDING: This study was funded by a research agreement from Eli Lilly and Company.

Hakozaki M, Ito S, Fujii T, et al.
Combined hepatocellular-cholangiocarcinoma with angiosarcomatoid change: A case report with immunohistochemical study.
Pathol Int. 2019; 69(2):110-116 [PubMed] Related Publications
Sarcomatoid combined hepatocellular-cholangiocarcinoma (cHCC-CCA) is a rare condition, with only 16 cases reported to date; however, there have been no reports of hepatic sarcomatoid carcinoma with angiosarcomatous features. Here, we report a rare case of cHCC-CCA with angiosarcomatoid changes in a 77-year-old man. The tumor was biphasic with malignant epithelial and mesenchymal components. Histologically, the epithelial component was concordant with classical type cHCC-CCA. The mesenchymal component included angiosarcomatoid cells growing in a vasoformative structure and undifferentiated spindle cells. Immunohistochemical analyses showed that angiosarcomatoid cells were positive for CD31, factor VIII-related antigen, and other angiosarcoma markers. Characteristically diffuse and strong expression of p53 protein was observed in the nuclei of angiosarcomatoid cells but not in carcinoma cells, suggesting that TP53 gene mutations commonly occur in these cells. Transitional zones were observed between HCC and spindle cells and between HCC and angiosarcomatoid cells. A small portion of undifferentiated spindle cells expressed pan-cytokeratin. These findings suggested that this extremely rare tumor developed from dedifferentiation or metaplastic changes of cHCC-CCA.

Wang T, Li W, Huang H, Wang C
Metastasis-Associated 1 (MTA1) Gene Expression Promotes Angiogenesis in Mouse Xenografts from Human Non-Small Cell Lung Cancer (NSCLC) Cells.
Med Sci Monit. 2019; 25:484-491 [PubMed] Free Access to Full Article Related Publications
BACKGROUND This study aimed to investigate the effects of metastasis-associated 1 (MTA1) gene expression and gene silencing in human non-small cell lung cancer (NSCLC) cells in vitro and on angiogenesis in tumor xenografts in vivo in nude mice. MATERIAL AND METHODS Human H460 and H1299 NSCLC cell lines underwent transfection with lentiviral transfer plasmids (lenti) and short-interfering RNA (si-RNA) and included a control group, a lenti-MTA1 group, a lenti-si-MTA1 group, a lenti control group, and a si-RNA control group. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) was used to detect MTA1 gene expression after cell transfection. MTA1 transfection was more effective in H460 cells, which were selected for further in vivo studies. Sixty Balb/c nude mice, containing human H460 cell tumor xenografts, included a control group (N=20), a lenti-MTA1 group (N=20), and a lenti-si-MTA1 group (N=20). Tumor tissue immunohistochemistry was used to detect the expression of MTA1 protein and microvessel density (MVD) using CD31. Western blot was used to quantify the expression of cyclooxygenase-2 (COX-2), angiopoietin 1/2 (Ang1/2), hypoxia-inducible factor 1-a (HIF-1a), and vascular endothelial growth factor (VEGF). RESULTS MTA1 silencing with si-RNA significantly reduced the tumor growth rate in nude mice (p<0.01), reduced tumor MVD, and 70% of mice survived for more than 30 days. MTA1 overexpression resulted in the death of all mice at 30 days after tumor inoculation and upregulated the expression of COX-2, Ang1/2, HIF-1a and VEGF, which were down-regulated by MTA1 silencing. CONCLUSIONS MTA1 gene expression promoted angiogenesis in mouse xenografts from human NSCLC cells.

Okamura S, Osaki T, Nishimura K, et al.
Thymidine kinase-1/CD31 double immunostaining for identifying activated tumor vessels.
Biotech Histochem. 2019; 94(1):60-64 [PubMed] Related Publications
Although angiogenesis plays a crucial role in cancer growth and progression, no reliable method for assessing angiogenesis in tumor tissue sections currently is available. Using biomarkers with high specificity for proliferating endothelial cells could help quantify angiogenic activity. Thymidine kinase-1 (TK1) is an enzyme involved in the salvage pathway of DNA synthesis and its activity is correlated with cell proliferation. We investigated the use of double immunostaining for TK1 and CD31 for identifying activated tumor vessels. Differences in TK1/CD31 positive vessel rates (PVRs) between tumor and adjacent normal tissues were evaluated in 39 colorectal carcinoma (CRC) samples and compared with those of Ki67/CD31 double stained tissues. Mean TK1/CD31 PVR (23.6%) in CRCs was 13.9 fold greater than in adjacent normal tissues (1.7%)). By comparison, mean Ki67/CD31 PVR in CRCs was 20.0%, i.e. only 4.8 fold greater than in normal tissues (4.2%). Also, mean TK1/CD31 PVR in normal tissues was significantly less than mean Ki67/CD31 PVR. Our findings indicate that double immunostaining for TK1/CD31 can detect activated tumor vessels more accurately than staining for Ki67/CD31 and potentially could identify tumors that will respond to anti-angiogenic therapy.

Bayat N, Izadpanah R, Ebrahimi-Barough S, et al.
The Anti-Angiogenic Effect of Atorvastatin in Glioblastoma Spheroids Tumor Cultured in Fibrin Gel: in 3D in Vitro Model
Asian Pac J Cancer Prev. 2018; 19(9):2553-2560 [PubMed] Free Access to Full Article Related Publications
Purpose: Glioblastoma multiform (GBM) is the most aggressive glial neoplasm. Researchers have exploited the fact that GBMs are highly vascularized tumors. Anti-angiogenic strategies including those targeting VEGF pathway have been emerged for treatment of GBM. Previously, we reported the anti-inflammatory effect of atorvastatin on GBM cells. In this study, we investigated the anti-angiogenesis and apoptotic activity of atorvastatin on GBM cells. Methods: Different concentrations of atorvastatin (1, 5, 10μM) were used on engineered three-dimensional (3D) human tumor models using glioma spheroids and Human Umbilical Vein Endothelial cells (HUVECs) in fibrin gel as tumor models. To reach for these aims, angiogenesis as tube-like structures sprouting of HUVECs were observed after 24 hour treatment with different concentrations of atorvastatin into the 3-D fibrin matrix and we focused on it by angiogenesis antibody array. After 48 hours exposing with different concentrations of atorvastatin, cell migration of HUVECs were investigated. After 24 and 48 hours exposing with different concentrations of atorvastatin VEGF, CD31, caspase-3 and Bcl-2 genes expression by real time PCR were assayed. Results: The results showed that atorvastatin has potent anti-angiogenic effect and apoptosis inducing effect against glioma spheroids. Atorvastatin down-regulated the expression of VEGF, CD31 and Bcl-2, and induced the expression of caspase-3 especially at 10μM concentration. These effects are dose dependent. Conclusion: These results suggest that this biomimetic model with fibrin may provide a vastly applicable 3D culture system to study the effect of anti-cancer drugs such as atorvastatin on tumor malignancy in vitro and in vivo and atorvastatin could be used as agent for glioblastoma treatment.

Liu Q, Fan D, Adah D, et al.
CRISPR/Cas9‑mediated hypoxia inducible factor‑1α knockout enhances the antitumor effect of transarterial embolization in hepatocellular carcinoma.
Oncol Rep. 2018; 40(5):2547-2557 [PubMed] Free Access to Full Article Related Publications
Transarterial embolization (TAE) is a palliative option commonly used for the treatment of advanced, unresectable hepatocellular carcinoma (HCC). However, patient prognosis in regards to overall survival has not improved with this method, mainly due to hypoxia‑inducible factor‑1α (HIF‑1α)‑induced angiogenesis and invasiveness. Thus, it is hypothesized that HIF‑1α may be an ideal knockout target for the treatment of HCC in combination with TAE. Thus, in the present study, HIF‑1α knockout was conducted in human liver cancer SMMC‑7721 cells and a xenograft HCC model was established using a lentivirus‑mediated CRISPR/Cas system (LV‑Cas) with small guide RNA‑721 (LV‑H721). Furthermore, hepatic artery ligation (HAL) was used to mimic human transarterial chemoembolization in mice. The results revealed that HIF‑1α was highly expressed in both HCC patient tissues and SMMC‑7721‑induced tumor tissues. The HIF‑1α knockout in SMMC‑7721 cells significantly suppressed cell invasiveness and migration, and induced cell apoptosis under CoCl2‑mimicking hypoxic conditions. Compared with the control groups, HAL + LV‑H721 inhibited SMMC‑7721 tumor growth in orthotopic HCC and markedly prolonged the survival of HCC‑bearing mice, which was accompanied by a lower CD31 expression (tumor angiogenesis) and increased apoptosis in the tumor cells. These findings demonstrated a valuable antitumor synergism in combining CRISPR/Cas9‑mediated HIF‑1α knockout with TAE in mice and highlighted the possibility that HIF‑1α may be an effective therapeutic knockout target in combination with TAE for HCC treatment.

Singhal J, Chikara S, Horne D, et al.
2'-Hydroxyflavanone inhibits in vitro and in vivo growth of breast cancer cells by targeting RLIP76.
Mol Carcinog. 2018; 57(12):1751-1762 [PubMed] Related Publications
Consumption of citrus-fruits is associated with reduced incidence of breast cancer (BC), the most common cancer diagnosed in women across the globe. In this study, we investigated the anticancer potential of 2-Hydroxyflavanone (2HF) in BC. 2HF, a citrus-bioflavonoid, has demonstrated anticancer properties in various cancers, but its anticancer role in BC has not been well studied. We investigated the in vitro and in vivo growth inhibitory effects of 2HF in an array of BC lines and in xenograft mouse models of ER-positive and HER2-positive BC cells. Compared to control, 2HF treatment reduced cell viability and suppressed migratory and invasive potential of BC cells, while, no growth inhibitory effects were observed in non-tumorigenic breast epithelial cells. Further, 2HF inhibited the expression of RLIP76, a stress-defensive and anti-apoptotic protein, which is over-expressed in BC cells and simultaneously reduced proliferation of BC cells. Nude mice bearing MCF7 or SKBR3 BC cells xenografts treated with either 2HF or targeting RLIP76 by RLIP76-antisense or RLIP76-antibody treatment had significantly lower tumor-weight as compared to corresponding controls. In addition, Western-blotting and immunohistochemical analysis of tumor tissue from control and treatment group mice showed that 2HF decreased protein expression levels of RLIP76, and the decrease was similar to those seen following RLIP76-antisense treatment. Furthermore, 2HF decreased expression of Ki67, CD31, vimentin, inhibited phosphorylation of Akt and expression of survivin and Bcl2, and increased levels of Bax, E-cadherin, and cleaved-PARP. Therefore, our results indicate that 2HF may suppress BC growth in vitro and in vivo by targeting RLIP76, and may serve as a potential adjuvant treatment in BC patients.

Lv Q, Wu K, Liu F, et al.
Interleukin‑17A and heparanase promote angiogenesis and cell proliferation and invasion in cervical cancer.
Int J Oncol. 2018; 53(4):1809-1817 [PubMed] Related Publications
Interleukin‑17A (IL‑17A) is a CD4 T-cell-derived pro-inflammatory cytokine that is involved in human cervical tumorigenesis. Heparanase (HPSE) is an endo-glycosidase expressed in mammals, which has been confirmed to be associated with cervical cancer invasion. In the present study, it was hypothesized that IL‑17A and HPSE are key proteins promoting tumor angiogenesis and cell proliferation and invasion in cervical cancer. The expression of IL‑17A and HPSE in cervical cancer tissues was detected by immunohistochemical staining. In addition, the expression of IL‑17A and HPSE was down- and upregulated via RNAi and human recombinant proteins, and MTT and Transwell assays were performed to examine cervical cancer cell proliferation and invasion, respectively. Flow cytometry analysis was also performed to detect cell cycle distribution, and the levels of target mRNA and protein were evaluated by reverse transcription-quantitative polymerase chain reaction and western blotting, respectively. IL‑17A and HPSE were highly expressed in cervical cancer tissues, and microvessel density was notably higher in the IL‑17A-positive group. IL‑17A and/or HPSE recombinant protein promoted the proliferation and invasion of cervical cancer cells, increased the proportion of cells in the G2/M phase, and enhanced the mRNA and protein expression of human papillomavirus E6, P53, vascular endothelial growth factor and CD31, whereas downregulation of IL‑17A and/or HPSE exerted the opposite effects. Furthermore, downregulation of IL‑17A and/or HPSE was found to inhibit the expression of nuclear factor (NF)-κB P65. In summary, IL‑17A and HPSE may promote tumor angiogenesis and cell proliferation and invasion in cervical cancer, possibly via the NF-κB signaling pathway. These findings may lead to the identification of new diagnostic markers and therapeutic targets.

Miao S, Qiu T, Zhao Y, et al.
Overexpression of S100A13 protein is associated with tumor angiogenesis and poor survival in patients with early-stage non-small cell lung cancer.
Thorac Cancer. 2018; 9(9):1136-1144 [PubMed] Free Access to Full Article Related Publications
BACKGROUND: S100A13 plays a key role in tumor growth and metastasis. The purpose of this study was to investigate the prognostic significance of S100A13 expression, microvessel density (MVD), and survival in early stage non-small cell lung cancer (NSCLC).
METHODS: In silico analysis was performed to determine the associations between S100A13 and NSCLC. The data of 82 patients with early-stage NSCLC who underwent radical resection were evaluated. Paraffin-embedded tumor specimens were stained with S100A13 and CD31 (a specific endothelial marker) using immunohistochemical methods. Prognostic significance was assessed by univariate and multivariate analyses.
RESULTS: S100A13 messenger RNA was overexpressed in NSCLC, especially in advanced stage. Of the 82 NSCLC specimens examined, 37 (45.1%) cases exhibited S100A13 overexpression and 31 (37.8%) showed high MVD. Univariate analysis indicated that gender, age, smoking status, histology type, tumor differentiation, and T stage were not significantly associated with prognosis. However, the overall and disease-free survival rates of patients with S100A13 overexpression and high MVD were significantly lower than in the remaining cases. Multivariate analysis demonstrated that only S100A13 overexpression was an independent factor for poor prognosis in early-stage NSCLC. Statistical analysis demonstrated that the MVD was significantly higher in tumors with high (67.6%, 25/37) compared to low S100A13 expression (13.3%, 6/45) (P < 0.01).
CONCLUSIONS: High S100A13 expression is closely associated with high intratumoral angiogenesis and poor prognosis in patients with stage I NSCLC. Immunohistochemical evaluation of S100A13 expression, along with an examination of the perioperative extent of angiolymphatic invasion, has value for predicting prognosis.

Luo D, Zhang X, Du R, et al.
Low dosage of arsenic trioxide (As
J Biol Inorg Chem. 2018; 23(6):939-947 [PubMed] Related Publications
Arsenic trioxide (As

Zuo H, Yang Q
The potential pathway of FOXC1 high expression in regulating the proliferation, migration, cell cycle and epithelialmesenchymal transition of basal-like breast cancer and in vivo imaging.
J BUON. 2018 May-Jun; 23(3):720-728 [PubMed] Related Publications
PURPOSE: To investigate the role of high forkhead box C1 (FOXC1) expression in basal-like breast cancer (BLBC) cells in vitro and in vivo, as well as its potential regulatory pathway.
METHODS: Stable MDA-MB-231 cells, a type of BLBC cells, with high FOXC1 expression and luciferase (FOXC1) were established. The parental MDA-MB-231 cells with luciferase served as the control group. Proliferation, migratory capabilities and the cell cycle were evaluated. The tumorigenicity and the spontaneous pulmonary metastasis were measured in mice in vivo. In vivo imaging was also performed. Histopathology, immunohistochemical analysis and microarray processing were evaluated. Paired Student's t-test was used.
RESULTS: The proliferation and migratory ability of FOXC1- MDA-MB-231 cells were enhanced significantly (p<0.05). Spontaneous pulmonary metastases were observed in 2 out of 5 mice, but no pulmonary metastases were observed in control animals. There were more FOXC1 cells in the G1 phase compared to the control (p<0.05), but there were also significant reductions of cells in the S and G2 phases (p<0.05). The CD31 and endoglin (CD105) expression in the FOXC1 tumor was higher than in the control, especially CD105 (p<0.05). The total fluorescence expression quantity of FOXC1 was higher than in the control cells (p<0.05), and the apparent diffusion coefficient (ADC) values were lower compared with the control (p<0.05). One pathway with the most gene enrichment (p38 MAPK signalling) may play a key role in regulating BLBC cell proliferation, migration, cell cycle and epithelial-mesenchymal transition (EMT) through the interaction of related critical regulatory genes (IL-6 and FOXC1).
CONCLUSION: High FOXC1 enhanced the proliferation, migratory ability and EMT of BLBC cells. This function may be regulated by IL-6 and FOXC1 through the p38 MAPK signalling pathway.

Lu J, Liu QH, Wang F, et al.
Exosomal miR-9 inhibits angiogenesis by targeting MDK and regulating PDK/AKT pathway in nasopharyngeal carcinoma.
J Exp Clin Cancer Res. 2018; 37(1):147 [PubMed] Free Access to Full Article Related Publications
BACKGROUND: Exosomes are small vesicles containing a wide range of functional proteins, mRNA and miRNA. Exosomal miRNAs from cancer cells play crucial roles in mediating cell-cell communication and tumor-microenvironment cross talk, specifically in enabling metastasis and promoting angiogenesis. We focused on miR-9 that was identified as a tumor suppressor previously in nasopharyngeal carcinoma (NPC) tumorigenesis.
METHODS: Differential centrifugation, transmission electron microscopy and nanoparticle tracking analysis were used to isolate and identify exosomes. Quantitative PCR and western blotting analysis were used to detect miR-9, pri-miR-9, CD63, TSG101, MDK, P70S6K P-Ser424 and PDK1 P-Ser241 expression. Laser confocal microscopy was used to trace exosomal miR-9 secreted by NPC cells into HUVECs. The effect of exosomal miR-9 on cell migration and tube formation of HUVECs in vivo and vitro was assessed by using migration assay, tube formation assay and matrigel plug assay, respectively. Bioinformatics analysis and luciferase reporter assay were utilized to confirm the binding of exosomal miR-9 to the 3'untranslated region (3'-UTR) of MDK, while Phosphorylation Array was performed to identify AKT Pathway in HUVECs treated with exosomal miR-9. Furthermore, Immunohistochemistry (IHC) and in situ hybridization (ISH) was used to detected miR-9, CD31 and MDK expression in human NPC tumor samples.
RESULTS: NPC cells transfected with miR-9-overexpressing lentivirus, released miR-9 in exosomes. Exosomal miR-9 directly suppressed its target gene - MDK in endothelial cells. Mechanistic analyses revealed that exosomal miR-9 from NPC cells inhibited endothelial tube formation and migration by targeting MDK and regulating PDK/AKT signaling pathway. Additionally, the level of MDK was upregulated in NPC tumor samples and was positively correlated with microvessel density. Notably, the level of exosomal miR-9 was positively correlated with overall survival, and MDK overexpression was positively associated with poor prognosis in NPC patients, suggesting the clinical relevance and prognostic value of exosomal miR-9 and MDK.
CONCLUSIONS: Taken together, our data identify an extracellular anti-angiogenic role for tumor-derived, exosome-associated miR-9 in NPC tumorigenesis and prompt further investigation into exosome-based therapies for cancer treatment.

Liang Y, Zhuo Y, Lin Z, et al.
Decreased Expression of MYPT1 Contributes to Tumor Angiogenesis and Poor Patient Prognosis in Human Prostate Cancer.
Curr Mol Med. 2018; 18(2):100-108 [PubMed] Free Access to Full Article Related Publications
BACKGROUND: Our previous study demonstrated that Myosin Phosphatase Targeting subunit 1 (MYPT1) may function as a direct target of microRNA-30d, which promotes tumor angiogenesis and tumor growth of prostate cancer (PCa). Here, we aimed to investigate the clinical significance of MYPT1 expression and its functions in PCa.
METHODS: Roles of MYPT1 deregulation in tumor angiogenesis of PCa was determined in vitro and in vivo experiments. Expression patterns of MYPT1 and CD31 proteins were examined by immunohistochemistry and immunofluorescence, respectively. Associations of MYPT1/CD31 combination with various clinicopathological features and patients' prognosis of PCa were also statistically evaluated.
RESULTS: Through gain- and loss-of-function experiments, MYPT1 inhibited capillary tube formation of endothelial cells and in vivo tumor angiogenesis in a mouse model with the downregulation of VEGF and CD31 expression. In addition, MYPT1 expression was significantly decreased, while CD31 expression was dramatically increased in PCa tissues compared to benign prostate tissues. Notably, MYPT1 expression levels in PCa tissues were negatively correlated with that of CD31. Statistically, MYPT1-low/CD31- high expression was distinctly associated with high Gleason score, positive biochemical recurrence, and reduced overall survival of PCa patients. Moreover, PCa patients with MYPT1-low/CD31-high expression more frequently had shorter overall, biochemical recurrence-free and metastasis-free survivals. MYPT1/CD31 combination was identified as an independent factor to predict biochemical recurrence-free and metastasis-free survivals of PCa patients.
CONCLUSIONS: Our findings indicate that MYPT1 may inhibit angiogenesis and contribute favorable prognosis in PCa patients, implying that MYPT1 might be a potential drug candidate in anticancer therapy.

Conti S, Vexler A, Edry-Botzer L, et al.
Combined acetyl-11-keto-β-boswellic acid and radiation treatment inhibited glioblastoma tumor cells.
PLoS One. 2018; 13(7):e0198627 [PubMed] Free Access to Full Article Related Publications
Glioblastoma multiforme (GBM) is the most common and most aggressive subtype of malignant gliomas. The current standard of care for newly diagnosed GBM patients involves maximal surgical debulking, followed by radiation therapy and temozolomide chemotherapy. Despite the advances in GBM therapy, its outcome remains poor with a median survival of less than two years. This poor outcome is partly due to the ability of GBM tumors to acquire adaptive resistance to therapy and in particular to radiation. One of the mechanisms contributing to GBM tumor progression and resistance is an aberrant activation of NF-ĸB, a family of inducible transcription factors that play a pivotal role in regulation of many immune, inflammatory and carcinogenic responses. Acetyl-11-keto-β-boswellic acid (AKBA) is a pentacyclic terpenoid extracted from the gum Ayurvedic therapeutic plant Boswellia serrata. AKBA is anti-inflammatory agent that exhibits potent cytotoxic activities against various types of tumors including GBM. One of the mechanisms underlying AKBA anti-tumor activity is its ability to modulate the NF-ĸB signaling pathway. The present study investigated in vitro and in vivo the effect of combining AKBA with ionizing radiation in the treatment of GBM and assessed AKBA anti-tumor activity and radio-enhancing potential. The effect of AKBA and/or radiation on the survival of cultured glioblastoma cancer cells was evaluated by XTT assay. The mode of interaction of treatments tested was calculated using CalcuSyn software. Inducing of apoptosis following AKBA treatment was evaluated using flow cytometry. The effect of combined treatment on the expression of PARP protein was analysed by Western blot assay. Ectopic (subcutaneous) GBM model in nude mice was used for the evaluation of the effect of combined treatment on tumor growth. Immunohistochemical analysis of formalin-fixed paraffin-embedded tumor sections was used to assess treatment-related changes in Ki-67, CD31, p53, Bcl-2 and NF-ĸB-inhibitor IĸB-α. AKBA treatment was found to inhibit the survival of all four tested cell lines in a dose dependent manner. The combined treatment resulted in a more significant inhibitory effect compared to the effect of treatment with radiation alone. A synergistic effect was detected in some of the tested cell lines. Flow cytometric analysis with Annexin V-FITC/PI double staining of AKBA treated cells indicated induction of apoptosis. AKBA apoptotic activity was also confirmed by PARP cleavage detected by Western blot analysis. The combined treatment suppressed tumor growth in vivo compared to no treatment and each treatment alone. Immunohistochemical analysis showed anti-angiogenic and anti-proliferative activity of AKBA in vivo. It also demonstrated a decrease in p53 nuclear staining and in Bcl-2 staining and an increase in IĸB-α staining following AKBA treatment both alone and in combination with radiotherapy. In this study, we demonstrated that AKBA exerts potent anti-proliferative and apoptotic activity, and significantly inhibits both the survival of glioblastoma cells in vitro and the growth of tumors generated by these cells. Combination of AKBA with radiotherapy was found to inhibit factors which involved in cell death regulation, tumor progression and radioresistence, therefore it may serve as a novel approach for GBM patients.

Cui L, Meng Q, Wen J, et al.
The effect of a gene associated with retinoid-interferon-induced mortality 19 (GRIM-19) on STAT3-induced gene expression in renal carcinoma.
J Biochem. 2018; 164(4):285-294 [PubMed] Related Publications
This study aimed to investigate the exact regulatory mechanisms of retinoid-interferon-induced mortality 19 (GRIM-19) in renal carcinoma. Tumour tissue samples from patients with renal carcinoma (n = 30, there were seven cases of Stage I, eight cases of Stage II, eight cases of Stage III, seven cases of Stage IV) and control subjects were selected from adjacent normal tissue (n = 10). Real-time quantitative PCR and western blotting were used to assess the level of GRIM-19, signal transducer and activator of transcription-3 (STAT3) and its downstream molecules. CD31 was detected by immunohistochemistry. The MTT assay was used to measure cell proliferation. The amount of apoptosis cells was analysed by Flow cytometry. The results showed that expression of GRIM-19 was decreased in renal carcinoma. However, in tumour tissue, STAT3 and its downstream signalling molecules showed the higher expression compared with control. Overexpression of GRIM-19, inhibited tumour growth apoptosis by mediating activators of STAT3 signal. In addition, interferon-β and all-trans-retinoic acid inhibited the renal carcinoma cell growth and induced apoptosis, and effect of drug combinations was particularly evident. In conclusion, GRIM-19 expression is associated with hyperactivation of STAT3-induced gene expression in renal carcinoma.

Hong S, Chen S, Wang X, et al.
ATAD2 silencing decreases VEGFA secretion through targeting has-miR-520a to inhibit angiogenesis in colorectal cancer.
Biochem Cell Biol. 2018; 96(6):761-768 [PubMed] Related Publications
ATPase family AAA domain-containing protein 2 (ATAD2) is involved in various types of cancers, including colorectal cancer. This study aimed to determine the role of ATAD2 in angiogenesis in colorectal cancer. Here, we downregulated ATAD2 expression in HCT116 and SW480 cells, and collected the conditioned medium (CM) from control and ATAD2-silenced cells. The effect of CM on human umbilical vein endothelial cells (HUVEC) was evaluated by using CCK-8, wound healing, tube formation, Western blot, and dual-luciferase reporter assays. Our results showed that the proliferation, migration, and tube formation of HUVEC were reduced in presence of ATAD2-silenced CM, and the levels of phosphorylated vascular endothelial growth factor receptor 2 (P-VEGFR2), CD31, and CD34 were downregulated. Mechanism studies showed that ATAD2 silencing regulated the expression of vascular endothelial growth factor A (VEGFA) and miR-520a. Moreover, we found that miR-520a could bind to ATAD2, and its inhibitor partly reversed the alterations in HUVEC induced by CM from ATAD2-silenced cells. In addition, we demonstrated that miR-520a directly bound to 3'-UTR of VEGFA and inhibited its expression. Collectively, our results indicate that ATAD2 inhibition suppresses VEGFA secretion by increasing miR-520a levels. Our study suggests ATAD2 as a potential therapeutic target for angiogenesis in colorectal cancer.

Ruscito I, Cacsire Castillo-Tong D, Vergote I, et al.
Characterisation of tumour microvessel density during progression of high-grade serous ovarian cancer: clinico-pathological impact (an OCTIPS Consortium study).
Br J Cancer. 2018; 119(3):330-338 [PubMed] Free Access to Full Article Related Publications
BACKGROUND: High-grade serous ovarian cancer (HGSOC) intratumoural vasculature evolution remains unknown. The study investigated changes in tumour microvessel density (MVD) in a large cohort of paired primary and recurrent HGSOC tissue samples and its impact on patients' clinico-pathological outcome.
METHODS: A total of 222 primary (pOC) and recurrent (rOC) intra-patient paired HGSOC were assessed for immunohistochemical expression of angiogenesis-associated biomarkers (CD31, to evaluate MVD, and VEGF-A). Expression profiles were compared between pOCs and rOCs and correlated with patients' data.
RESULTS: High intratumoural MVD and VEGF-A expression were observed in 75.7% (84/111) and 20.7% (23/111) pOCs, respectively. MVD
CONCLUSIONS: HGSOC intratumoural vasculature did not undergo significant changes during disease progression. High concentration of CD31

Mishra A, Sriram H, Chandarana P, et al.
Decreased expression of cell adhesion genes in cancer stem-like cells isolated from primary oral squamous cell carcinomas.
Tumour Biol. 2018; 40(5):1010428318780859 [PubMed] Related Publications
The goal of this study was to isolate cancer stem-like cells marked by high expression of CD44, a putative cancer stem cell marker, from primary oral squamous cell carcinomas and identify distinctive gene expression patterns in these cells. From 1 October 2013 to 4 September 2015, 76 stage III-IV primary oral squamous cell carcinoma of the gingivobuccal sulcus were resected. In all, 13 tumours were analysed by immunohistochemistry to visualise CD44-expressing cells. Expression of CD44 within The Cancer Genome Atlas-Head and Neck Squamous Cell Carcinoma RNA-sequencing data was also assessed. Seventy resected tumours were dissociated into single cells and stained with antibodies to CD44 as well as CD45 and CD31 (together referred as Lineage/Lin). From 45 of these, CD44

Hutchenreuther J, Vincent K, Norley C, et al.
Activation of cancer-associated fibroblasts is required for tumor neovascularization in a murine model of melanoma.
Matrix Biol. 2018; 74:52-61 [PubMed] Related Publications
Metastatic melanoma is highly fatal. Within the tumor microenvironment, the role of cancer-associated fibroblasts (CAFs) in melanoma metastasis and progression is relatively understudied. The matricellular protein CCN2 (formerly termed connective tissue growth factor, CTGF) is overexpressed, in a fashion independent of BRAF mutational status, by CAFs in melanoma. Herein, we find, in human melanoma patients, that CCN2 expression negatively correlates with survival and positively correlates with expression of neovascularization markers. To assess the role of CAFs in melanoma progression, we used C57BL/6 mice expressing a tamoxifen-dependent cre recombinase expressed under the control of a fibroblast-specific promoter/enhancer (COL1A2) to delete CCN2 postnatally in fibroblasts. Mice deleted or not for CCN2 in fibroblasts were injected subcutaneously with B16-F10 melanoma cells. Loss of CCN2 in CAFs resulted in reduced CAF activation, as detected by staining with anti-α-smooth muscle actin antibodies, and reduced tumor-induced neovascularization, as detected by micro-computed tomography (micro-CT) and staining with anti-CD31 antibodies. CCN2-deficient B16(F10) cells were defective in a tubule formation/vasculogenic mimicry assay in vitro. Mice deleted for CCN2 in CAFs also showed impaired vasculogenic mimicry of subcutaneously-injected B16-F10 cells in vivo. Our results provide new insights into the cross-talk among different cell types in the tumor microenvironment and suggest CAFs play a heretofore unappreciated role by being essential for tumor neovascularization via the production of CCN2. Our data are consistent with the hypothesis that activated CAFs are essential for melanoma metastasis and that, due to its role in this process, CCN2 is a therapeutic target for melanoma.

Lin Y, Liu S, Su L, et al.
miR-570 Inhibits Proliferation, Angiogenesis, and Immune Escape of Hepatocellular Carcinoma.
Cancer Biother Radiopharm. 2018; 33(6):252-257 [PubMed] Related Publications
Hepatocellular carcinoma (HCC) is one common malignancy. The authors previously demonstrated that miR-570 regulates the development of HCC. This study detected the effect of miR-570 on cell apoptosis, angiogenesis, T cell activation, and proliferation in a tumorigenicity assay in nude mice. miR-570 mimics and negative control (NC) were transfected into SMMC7721 cells, and then, the cells were subcutaneously injected in the right flank in nude mice. Six weeks later, the dissected tumors and peripheral blood were collected. Tumor weight and volume were measured, and expression of miR-570 and apoptosis-related gene Bax/Bcl-2 was detected by quantitative real-time polymerase chain reaction. Hematoxylin and eosin, immunohistochemistry of CD31 and vascular endothelial growth factor (VEGF), TUNEL assay, and flow cytometry detection of CD4 and CD8 in peripheral blood were performed. miR-570 mimics suppressed tumor growth compared with the NC, with decreases in tumor weight and tumor volume. Very few CD31 and VEGF were found in tumor sections in miR-570 mimics group. Bax level was significantly increased, while Bcl-2 level was significantly downregulated. Significant lower ratio of CD3

Lin J, Cao S, Wang Y, et al.
Long non-coding RNA UBE2CP3 enhances HCC cell secretion of VEGFA and promotes angiogenesis by activating ERK1/2/HIF-1α/VEGFA signalling in hepatocellular carcinoma.
J Exp Clin Cancer Res. 2018; 37(1):113 [PubMed] Free Access to Full Article Related Publications
BACKGROUND: Angiogenesis is considered as an important process in the development of malignancies and is associated with cancer progression and metastasis. Hepatocellular carcinoma (HCC) is the most common primary tumor of the liver and is recognized as a typical angiogenic tumor. Thus, it is of great importance to study the underlying mechanism of angiogenesis in HCC. The long non-coding RNA (lncRNA) ubiquitin conjugating enzyme E2C pseudogene 3 (UBE2CP3) has been reported as an oncogene that promotes tumor metastasis in HCC. However, the role and underlying mechanisms of UBE2CP3 in HCC angiogenesis are still unclear.
METHODS: We measured the expression levels of UBE2CP3 by in situ hybridization (ISH) and quantitative real-time polymerase chain reaction (qRT-PCR) in HCC patient samples. We also concomitantly used CD31/PAS double-staining to measure endothelial vessel (EV) density and used qRT-PCR to measure the CD31 mRNA level. HepG2 and SMMC-7721 cells were transfected with Lv-UBE2CP3 or Sh-UBE2CP3 virus to obtain stably over-expressing or knocking-down UBE2CP3 cell lines. The indirect effects of UBE2CP3 on ECs were studied by establishing a co-culture system using Transwell chambers with a 0.4-μm pore size. HCC cells and ECs in the co-culture system were separated, but the cytokines and growth factors were able to communicate with each other. Following exposed to HCC cells, ECs were collected for functional studies. Finally, we studied the function of UBE2CP3 in vivo by chick embryo chorioallantoic membrane (CAM) angiogenesis assays and nude mouse tumorigenicity assays.
RESULTS: In this study, we found that UBE2CP3 expression was higher in HCC tissues than in para-tumor tissues and was up-regulated in tissues with high EV density. Functionally, we found that in the co-culture systems, HCC cells overexpressing UBE2CP3 promoted HUVEC proliferation, migration and tube formation via the activation of ERK/HIF-1α/p70S6K/VEGFA signalling, increasing the level of VEGFA in HCC cell supernatant. In addition, the opposite results appeared when the expression of UBE2CP3 in HCC cells was knocked down. Consistent with these results, CAM angiogenesis assays and nude mouse tumorigenicity assays showed that UBE2CP3 expression up-regulated EV density in vivo.
CONCLUSION: Our study suggests that UBE2CP3 can enhance the interaction between HCC tumor cells and HUVECs and promote HCC tumorigenicity by facilitating angiogenesis.

Kim IK, Park SO, Chang H, Jin US
Inhibition Mechanism of Acellular Dermal Matrix on Capsule Formation in Expander-Implant Breast Reconstruction After Postmastectomy Radiotherapy.
Ann Surg Oncol. 2018; 25(8):2279-2287 [PubMed] Related Publications
BACKGROUND: Capsular contracture is one of the most common complications of expander-implant breast reconstruction. Recently, clinical reports have shown that use of an acellular dermal matrix (ADM) to cover breast implants decreases incidence of capsular contracture, but the underlying mechanism is unclear. Here, we examine how ADM reduces capsular formation in expander-implant breast reconstruction and identify cellular and molecular mechanisms of ADM-mediated reduction of capsular contracture in nonirradiated and irradiated patients.
METHODS: Thirty patients who underwent immediate two-stage implant-based breast reconstruction were included; 15 received radiotherapy. While the tissue expander was changed to permanent silicone implant, biopsies of the subpectoral capsule and ADM capsule were performed. Capsule thickness, immunohistochemistry of α-smooth muscle actin (αSMA), vimentin, CD31, F4/80 expression, αSMA and CD31 coexpression, and relative gene expression levels of transforming growth factor (TGF)-β1 and platelet-derived growth factor (PDGF)-B were investigated.
RESULTS: Irradiated submuscular capsules were thicker than nonirradiated submuscular capsules, but the thickness of ADM capsules did not significantly differ between nonirradiated and irradiated groups. Levels of myofibroblasts, fibroblasts, vascularity, EndoMT, and macrophages were significantly lower in ADM capsules than in submuscular capsules. With the exception of EndoMT, all others were increased in irradiated submuscular capsules compared with nonirradiated submuscular capsule, while none significantly differed between nonirradiated and irradiated ADM capsules.
CONCLUSIONS: Use of ADM reduced myofibroblasts, vascularity, fibroblasts, and EndoMT in capsule tissues. Moreover, ADM use decreased macrophages, a key regulator of tissue fibrosis, as well as TGF-β1 and PDGF-B expression. We hope that these results provide basic concepts important for prevention of capsular contracture.

Rusak A, Jablonska K, Piotrowska A, et al.
The Role of CHI3L1 Expression in Angiogenesis in Invasive Ductal Breast Carcinoma.
Anticancer Res. 2018; 38(6):3357-3366 [PubMed] Related Publications
BACKGROUND/AIM: An increased level of chitinase 3 like 1 protein (CHI3L1) expression is observed in patients with cancer and may have potential prognostic value. The aim of this study was to evaluate the role of CHI3L1 in angiogenesis in invasive ductal breast carcinoma (IDC) (n=110).
MATERIALS AND METHODS: Immunohistochemistry was used to assess the expression of CHI3L1, CD31, CD34, vascular endothelial growth factor (VEGFA, VEGFC and VEGFD). Real-time polymerase chain reaction and western blot were used to determine the level of CHI3L1 mRNA and protein.
RESULTS: Immunohistochemistry demonstrated positive correlation between CHI3L1 expression and angiogenesis markers: CD31 (r=0.34, p=0.0003), CD34 (r=0.24, p=0.012), VEGFD (r=0.24, p=0.013). Higher CHI3L1 expression in estrogen receptor-negative (p=0.041) and progesterone receptor-negative (p=0.014) cancer was observed. Higher CHI3L1 expression was reported in cancer tissues in comparison to non-malignant breast lesions.
CONCLUSION: These results suggest a potential role of CHI3L1 in angiogenesis in IDC and may suggest its involvement in cancer progression.

Crespo J, Wu K, Li W, et al.
Human Naive T Cells Express Functional CXCL8 and Promote Tumorigenesis.
J Immunol. 2018; 201(2):814-820 [PubMed] Free Access to Full Article Related Publications
Naive T cells are thought to be functionally quiescent. In this study, we studied and compared the phenotype, cytokine profile, and potential function of human naive CD4

Pucci A, Mattioli C, Matteucci M, et al.
Cell differentiation in cardiac myxomas: confocal microscopy and gene expression analysis after laser capture microdissection.
Heart Vessels. 2018; 33(11):1403-1410 [PubMed] Related Publications
Cardiac myxomas are rare tumors with a heterogeneous cell population including properly neoplastic (lepidic), endothelial and smooth muscle cells. The assessment of neoplastic (lepidic) cell differentiation pattern is rather difficult using conventional light microscopy immunohistochemistry and/or whole tissue extracts for mRNA analyses. In a preliminary study, we investigated 20 formalin-fixed and paraffin-embedded cardiac myxomas by means of conventional immunohistochemistry; in 10/20 cases, cell differentiation was also analyzed by real-time RT-PCR after laser capture microdissection of the neoplastic cells, whereas calretinin and endothelial antigen CD31 immunoreactivity was localized in 4/10 cases by double immunofluorescence confocal microscopy. Gene expression analyses of α-smooth muscle actin, endothelial CD31 antigen, alpha-cardiac actin, matrix metalloprotease-2 (MMP2) and tissue inhibitor of matrix metalloprotease-1 (TIMP1) was performed on cDNA obtained from either microdissected neoplastic cells or whole tumor sections. We found very little or absent CD31 and α-Smooth Muscle Actin expression in the microdissected cells as compared to the whole tumors, whereas TIMP1 and MMP2 genes were highly expressed in both ones, greater levels being found in patients with embolic phenomena. α-Cardiac Actin was not detected. Confocal microscopy disclosed two different signals corresponding to calretinin-positive myxoma cells and to endothelial CD31-positive cells, respectively. In conclusion, the neoplastic (lepidic) cells showed a distinct gene expression pattern and no consistent overlapping with endothelial and smooth muscle cells or cardiac myocytes; the expression of TIMP1 and MMP2 might be related to clinical presentation; larger series studies using also systematic transcriptome analysis might be useful to confirm the present results.

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