Locus Summary

Gene:MIR107; microRNA 107
Aliases: MIRN107, miR-107
Summary:microRNAs (miRNAs) are short (20-24 nt) non-coding RNAs that are involved in post-transcriptional regulation of gene expression in multicellular organisms by affecting both the stability and translation of mRNAs. miRNAs are transcribed by RNA polymerase II as part of capped and polyadenylated primary transcripts (pri-miRNAs) that can be either protein-coding or non-coding. The primary transcript is cleaved by the Drosha ribonuclease III enzyme to produce an approximately 70-nt stem-loop precursor miRNA (pre-miRNA), which is further cleaved by the cytoplasmic Dicer ribonuclease to generate the mature miRNA and antisense miRNA star (miRNA*) products. The mature miRNA is incorporated into a RNA-induced silencing complex (RISC), which recognizes target mRNAs through imperfect base pairing with the miRNA and most commonly results in translational inhibition or destabilization of the target mRNA. The RefSeq represents the predicted microRNA stem-loop. [provided by RefSeq, Sep 2009]
Databases:miRBase, OMIM, HGNC, Ensembl, GeneCard, Gene
Source:NCBIAccessed: 14 March, 2017

Cancer Overview

Research Indicators

Publications Per Year (1992-2017)
Graph generated 14 March 2017 using data from PubMed using criteria.

Literature Analysis

Mouse over the terms for more detail; many indicate links which you can click for dedicated pages about the topic.

Tag cloud generated 14 March, 2017 using data from PubMed, MeSH and CancerIndex

Specific Cancers (11)

Data table showing topics related to specific cancers and associated disorders. Scope includes mutations and abnormal protein expression.

Note: list is not exhaustive. Number of papers are based on searches of PubMed (click on topic title for arbitrary criteria used).

MicroRNA Function

Numbers shown below represent number of publications held in OncomiRDB database for Oncogenic and Tumor-Suppressive MicroRNAs.

TissueTarget Gene(s)Regulator(s)MIR107 Function in CancerEffect
stomach (2)
-gastric cancer (2)
CDK6 (1)
DICER1 (1)
inhibit cell proliferation (1)
induce cell cycle G1 arrest (1)
inhibit cell invasion (1)
promote cell migration (1)
promote cell invasion (1)
tumor-suppressive (1)
oncogenic (1)
blood (2)
-chronic lymphocytic leukemia (1)
-acute promyelocytic leukemia (1)
PLAG1 (1)
NFIA (1)
all-trans-retinoic a (1)
tumor-suppressive (1)
colorectum (2)
-colorectal cancer (1)
-colon cancer (1)
DAPK1 (1)
ARNT (1)
KLF4 (1)
TP53 (1)
increase cell motility (1)
increase cell-matrix adhesion (1)
decrease cell-cell adhesion (1)
inhibit hypoxic signaling (1)
suppress tumor angiogenesis (1)
suppress tumor growth (1)
oncogenic (1)
tumor-suppressive (1)
head and neck (2)
-head and neck squamous cell carcinoma (2)
inhibit cell invasion (2)
reduce clonogenic survival (1)
inhibit cell migration (1)
reduce the cancer-initiating cell population (1)
inhibit tumor growth (1)
inhibit cell proliferation (1)
inhibit DNA replication (1)
inhibit colony formation (1)
tumor-suppressive (2)
brain (1)
-glioma (1)
TP53 (1)
inhibit cell proliferation (1)
induce cell cycle arrest at the G0-G1 phase (1)
tumor-suppressive (1)
breast (1)
-breast cancer stem-like cells (1)
SUZ12 (1)
ZEB1 (1)
ZEB2 (1)
inhibit cancer stem cell growth (1)
tumor-suppressive (1)
pituitary (1)
-pituitary adenoma (1)
inhibit cell proliferation (1)
tumor-suppressive (1)
lung (1)
-non-small cell lung cancer (1)
inhibit cell growth (1)
induce cell cycle G1 arrest (1)
tumor-suppressive (1)
pancreas (1)
-pancreatic cancer (1)
inhibit cell growth (1)
tumor-suppressive (1)

Source: OncomiRDB Wang D. et al. Bioinformatics 2014, 30(15):2237-2238.

Latest Publications: MIR107 (cancer-related)

Zhang Y, Li T, Qiu Y, et al.
Serum microRNA panel for early diagnosis of the onset of hepatocellular carcinoma.
Medicine (Baltimore). 2017; 96(2):e5642 [PubMed] Free Access to Full Article Related Publications
Unique change of circulating microRNAs (miRNAs) was recognized to occur in early oncogenesis, which conferred it the potential as biomarkers for early detection of cancer. However, its diagnostic capability for hepatocellular carcinoma (HCC) has not been fully understood. In this study, microarray analysis was applied to screen the initial candidate miRNA from both the supernatants of anoikis-resistant cellular models and the sera samples of HCC patients. The selected differentially expressed miRNAs were further verified in 115 HCC patients and 40 health controls by qRT-PCR. Among these, 4 miRNAs (miR-16-2-3p, 92a-3p, 107, and 3126-5p) were significantly changed in HCC patients compared with controls. Logistic regression analysis identified a 3-miRNA panel (miR-92-3p, miR-107, and miR-3126-5p) as valuable diagnostic marker for HCC, especially for early stage patients (AUC = 0.975) and for low-level AFP HCC patients (AUC = 0.971). In addition, the combination of 3-miRNA panel and AFP was even more effective for discriminating the early stage HCC patients (AUC = 0.988) and low-level AFP HCC patients (AUC = 0.989) from control. In conclusion, diagnostic efficacy of the combination of 3-miRNA panel and AFP was powerful for HCC diagnosis, especially in early tumor screening and low-level AFP patients.

Oze I, Shimada S, Nagasaki H, et al.
Plasma microRNA-103, microRNA-107, and microRNA-194 levels are not biomarkers for human diffuse gastric cancer.
J Cancer Res Clin Oncol. 2017; 143(3):551-554 [PubMed] Related Publications
PURPOSE: Diffuse-type gastric cancer (DGC) carries a poor prognosis. Effective screening is one measure that might improve the prognosis of this disease. An E-cadherin/p53 double-conditional knockout (DCKO) mouse line recapitulates human DGC morphologically and molecularly. Three circulating microRNAs (miRNA) (miR-103, miR-107, miR-194) in DCKO mice have been identified as biomarkers for DGC. We sought to evaluate whether these circulating miRNAs could be used for the detection of human DGC.
METHODS: Subjects were 50 patients with DGC. Controls were first-time outpatients at Aichi Cancer Center Hospital, age- and sex-matched, without a cancer diagnosis. Total RNA containing miRNA was extracted from the plasma samples and then reverse-transcribed. The levels of miRNAs in plasma samples were quantitatively determined by real-time RT-PCR. Spiked-in cel-miR-39 was analyzed as a normalization control.
RESULTS: Levels of the three plasma microRNA levels in DGC cases with or without an intestinal component were not significantly different from those in control subjects. The areas under the receiver operating characteristic curve of miR-103, miR-107, and miR-194 were 0.548, 0.563, and 0.512, respectively.
CONCLUSIONS: In contrast to the DCKO mouse model, plasma miR-103, miR-107, and miR-194 levels are not altered in DGC and are not suitable for human DGC screening.

Zou C, Zou C, Cheng W, et al.
Heme oxygenase-1 retards hepatocellular carcinoma progression through the microRNA pathway.
Oncol Rep. 2016; 36(5):2715-2722 [PubMed] Related Publications
Heme metabolism system is involved in microRNA (miRNA) biogenesis. The complicated interplay between heme oxygenase-1 (HO-1) and miRNA has been observed in various tissues and diseases, including human malignancy. In the present study, our data showed that stable HO-1 overexpression in hepatocellular carcinoma (HCC) cells downregulated several oncomiRs. The most stably downregulated are miR-30d and miR-107. Iron, one of HO-1 catalytic products, was an important mediator in this regulation. Cell function analysis demonstrated that HO-1 inhibited the proliferation and metastasis of HepG2 cells, whereas miR-30d/miR-107 improved the proliferative and migratory ability of HepG2 cells. The beneficial effect of HO-1 in HCC inhibition could be reversed by upregulating miR-30d and miR-107. Akt and ERK pathways may be involved in the regulation of HO-1/miR-30d/miR-107 in HCC. These data indicate that HO-1 significantly suppresses HCC progression by regulating the miR-30d/miR-107 level, suggesting miR-30d/miR-107 regulation as a new molecular mechanism of HO-1 anticancer effect.

Datta J, Islam M, Dutta S, et al.
Suberoylanilide hydroxamic acid inhibits growth of head and neck cancer cell lines by reactivation of tumor suppressor microRNAs.
Oral Oncol. 2016; 56:32-9 [PubMed] Article available free on PMC after 01/05/2017 Related Publications
BACKGROUND: microRNAs negatively regulate gene expression at the post-transcriptional level. Mounting evidence shows that miR expression is deregulated in human cancers including head and neck squamous cell carcinoma (HNSCC). Epigenetically silenced tumor suppressor miRs may be re-expressed upon treatment with histone deacetylases inhibitors. Suberoylanilide Hydroxamic Acid (SAHA) is a histone deacetylase inhibitor that is currently being investigated in clinical trials for HNSCC. We hypothesized that SAHA will re-express a set of tumor suppressor miRs and enhance the efficacy of cisplatin and radiation in HNSCC.
RESULTS: In this study, miR expression profile was utilized to identify the tumor suppressor miRs that are re-expressed following SAHA treatment in HNSCC. Our data demonstrated that two tumor suppressor miRs, miR-107 and miR-138, were significantly up-regulated in CAL27 and SCC25 cell lines, following SAHA treatment. In addition to this, treatment with SAHA in a dose dependent manner significantly inhibited the cell proliferation, cell migration, and anchorage dependent clonogenic survival in CAL27 and SCC25 cell lines, respectively. Further, the expression of several oncogenes, PKCε, HIF1β, CDK6, and RhoC were down regulated in response to SAHA treatment. Additionally, we demonstrated that the combination treatment with SAHA and a chemotherapeutic drug cisplatin caused a significant reduction of cell growth compared to the single agent treatment.
CONCLUSION: Our data indicate that SAHA treatment results in reactivation of the silenced tumor suppressor miRs. Furthermore, this study emphasizes the usefulness of this drug as a novel combination therapy for HNSCC patients.

Wang P, Wu T, Zhou H, et al.
Long noncoding RNA NEAT1 promotes laryngeal squamous cell cancer through regulating miR-107/CDK6 pathway.
J Exp Clin Cancer Res. 2016; 35:22 [PubMed] Article available free on PMC after 01/05/2017 Related Publications
BACKGROUND: Long noncoding RNA nuclear paraspeckle assembly transcript 1 (NEAT1) plays key role in the progression of some human cancers. However, the role of NEAT1 in human laryngeal squamous cell cancer (LSCC) is still unknown. We therefore investigated the expression and function of NEAT1 in LSCC.
METHODS: NEAT1 level in LSCC and adjacent non-neoplastic tissues were detected by qRT-PCR. NEAT1 was knockdown in LSCC cells and cell proliferation, apoptosis and cell cycle were examined. The growth of xenografts with NEAT1 knockdown LSCC cells was analyzed.
RESULTS: NEAT1 level was significantly higher in LSCC than in corresponding adjacent non-neoplastic tissues, and patients with neck nodal metastasis or advanced clinical stage had higher NEAT1 expression. Moreover, siRNA mediated NEAT1 knockdown significantly inhibited the proliferation and induced apoptosis and cell cycle arrest at G1 phase in LSCC cells. The growth of LSCC xenografts was significantly suppressed by the injection of NEAT1 siRNA lentivirus. Furthermore, NEAT1 regulated CDK6 expression in LSCC cells which was mediated by miR-107.
CONCLUSION: NEAT1 plays an oncogenic role in the tumorigenesis of LSCC and may serve as a potential target for therapeutic intervention.

Cui J, Mo J, Luo M, et al.
c-Myc-activated long non-coding RNA H19 downregulates miR-107 and promotes cell cycle progression of non-small cell lung cancer.
Int J Clin Exp Pathol. 2015; 8(10):12400-9 [PubMed] Article available free on PMC after 01/05/2017 Related Publications
To verify c-Myc can regulate the expression of lncRNA H19 directly in non-small cell lung cancer (NSCLC) and clarify the molecular mechanism on how lncRNA H19 promote the cell cycle progression of NSCLC. The mRNA levels of lncRNA H19 in NSCLC tissues and cells, the adjacent tissues and normal cells were determined by RT-PCR. The expression change of lncRNA H19 in NSCLC cells after transfection with pcDNA3.1-c-Myc or c-Myc-siRNA was determined by RT-PCR, respectively. Targeted role of c-Myc on the promoter of H19 was studied by luciferase reporter assay. Chromosome immune coprecipitation (ChIP) was used to confirm the relationship between c-Myc and H19. MiRNAs that have base-pairing with H19 was predicted by online software. The relationship between H19 and miR-107 was determined by disturbing and overexpressing the expression of H19. The influence of the changes of H19 and miR-107 on cell cycle progression was determined by flow cytometry. The mRNA levels of lncRNA H19 in NSCLC tissues and cells were significantly higher than the adjacent tissues and normal cells, respectively. The expression of H19 increased or decreased accordingly with the overexpression and knockdown of c-Myc. The activity of the promoter of H19 was strengthened by c-Myc. While the expression of miR-107 increased or decreased with the overexpression and knockdown of H19, respectively. The number of cells in G2/M stage decreased significantly with the knockdown of H19 and miR-107 compared with the control group. Our study demonstrates that lncRNA H19, which is induced by c-Myc, is up-regulated in NSCLC. H19 influences the mitotic progression of NSCLC cell lines.

Teng R, Hu Y, Zhou J, et al.
Overexpression of Lin28 Decreases the Chemosensitivity of Gastric Cancer Cells to Oxaliplatin, Paclitaxel, Doxorubicin, and Fluorouracil in Part via microRNA-107.
PLoS One. 2015; 10(12):e0143716 [PubMed] Article available free on PMC after 01/05/2017 Related Publications
Higher Lin28 expression is associated with worse pathologic tumor responses in locally advanced gastric cancer patients undergoing neoadjuvant chemotherapy. However, the characteristics of Lin28 and its mechanism of action in chemotherapy resistance is still unclear. In this study, we found that transfection of Lin28 into gastric cancer cells (MKN45 and MKN28) increased their resistance to the chemo-drugs oxaliplatin (OXA), paclitaxel (PTX), doxorubicin (ADM), and fluorouracil (5-Fu) compared with gastric cancer cells transfected with a control vector. When knockdown Lin28 expression by Lin28 small interfering RNA (siRNA) was evaluated in vitro, we found that the resistance to chemo-drugs was reduced. Furthermore, we found that Lin28 up-regulates C-myc and P-gp and down-regulates Cylin D1. Finally, we found that miR-107 is a target microRNA of Lin28 and that it participates in the mechanism of chemotherapy resistance. Our results suggest that the Lin28/miR-107 pathway could be one of many signaling pathways regulated by Lin28 and associated with gastric cancer chemo-resistance.

Lu Z, Xiao Z, Liu F, et al.
Long non-coding RNA HULC promotes tumor angiogenesis in liver cancer by up-regulating sphingosine kinase 1 (SPHK1).
Oncotarget. 2016; 7(1):241-54 [PubMed] Article available free on PMC after 01/05/2017 Related Publications
Highly up-regulated in liver cancer (HULC) is a long non-coding RNA (lncRNA). We found that HULC up-regulated sphingosine kinase 1 (SPHK1), which is involved in tumor angiogenesis. Levels of HULC were positively correlated with levels of SPHK1 and its product, sphingosine-1-phosphate (S1P), in patients HCC samples. HULC increased SPHK1 in hepatoma cells. Chicken chorioallantoic membrane (CAM) assays revealed that si-SPHK1 remarkably blocked the HULC-enhanced angiogenesis. Mechanistically, HULC activated the promoter of SPHK1 in hepatoma cells through the transcription factor E2F1. Chromatin immunoprecipitation (ChIP) and electrophoretic mobility shift assay (EMSA) further showed that E2F1 was capable of binding to the E2F1 element in the SPHK1 promoter. HULC increased the expression of E2F1 in hepatoma cells and levels of HULC were positively correlated with those of E2F1 in HCC tissues. Intriguingly, HULC sequestered miR-107, which targeted E2F1 mRNA 3'UTR, by complementary base pairing. Functionally, si-SPHK1 remarkably abolished the HULC-enhanced tumor angiogenesis in vitro and in vivo. Taken together, we conclude that HULC promotes tumor angiogenesis in liver cancer through miR-107/E2F1/SPHK1 signaling. Our finding provides new insights into the mechanism of tumor angiogenesis.

Yang X, Wu X
miRNA expression profile of vulvar squamous cell carcinoma and identification of the oncogenic role of miR-590-5p.
Oncol Rep. 2016; 35(1):398-408 [PubMed] Related Publications
MicroRNAs (miRNAs), a class of small non-coding RNA molecules, are associated with a variety of human cancers. Currently, little data are available regarding miRNA expression in vulvar squamous cell carcinoma (VSCC); the mechanism of action of miRNAs in VSCC still requires investigation. The aim of the present study was to investigate the miRNA expression profile in VSCC using a miRCURY™ LNA array. The expression levels of selected miRNAs were quantified by RT-qPCR. The relationship between miR-590-5p expression and clinical pathology was assessed. The expression levels of crucial transforming growth factor-β (TGF-β) and Smad pathway factors were detected. We further investigated the role of miR-590-5p via in vitro studies in the A431 human VSCC cell line. A total of 157 miRNAs showed significantly altered expression in this type of carcinoma. Of particular interest, miR-590-5p, miR-182-5p and miR-183-5p were upregulated, and miR-603, miR-103a-3p and miR-107 were downregulated. A positive relationship was found between miR-590-5p expression and lymph node metastasis. In VSCC, TGFβ1 and TGFβ2 were significantly overexpressed and TGFβRII and Smad4 were significantly underexpressed at both the RNA and protein levels. In A431 cells, overexpression of miR-590-5p promoted proliferation, migration and G1-S phase transition and downregulated TGFβRII. The knockdown of TGFβRII by siRNA promoted malignant behaviours in the A431 cells. In conclusion, we present the miRNA expression profile in VSCC, and our findings suggest that the upregulation of miR-590-5p promotes cellular malignant behaviours via the target gene TGFβRII.

Ayremlou N, Mozdarani H, Mowla SJ, Delavari A
Increased levels of serum and tissue miR-107 in human gastric cancer: Correlation with tumor hypoxia.
Cancer Biomark. 2015; 15(6):851-60 [PubMed] Related Publications
BACKGROUND: MicroRNAs can function as oncogenes and tumor suppressor genes in human cancers. The expression of miR-107 is high in various types of solid tumors.
OBJECTIVE: The aim of this study was to evaluate the tumor and serum level of miR-107 and its correlation to HIF-1α expression in gastric cancer patients.
METHODS: Quantitative real-time PCR was used to analyze the expression of miR-107 and HIF-1α in 36 pairs of fresh gastric cancer and matched adjacent normal tissue specimens and the serum of these patients compared to age matched controls.
RESULTS: The expression level of miR-107 was significantly higher in tumor tissues compared to adjacent normal tissue (p= 0.04). For serum, the expression level of miR-107 was significantly higher in gastric cancer patients than in age matched controls (p= 0.04). The correlation between tumor and serum expression of miR-107 with tumor hypoxia was found to be significant (p≤ 0.001).
CONCLUSION: The overexpression of miR-107 in tumors and serum of gastric cancer patients and its correlation with HIF-1α expression in tumor tissues was indicated that miR-107 may have a potential to use as a biomarker for detection of gastric cancer patients and hypoxia in gastric cancer tumor.

Chen WS, Yen CJ, Chen YJ, et al.
miRNA-7/21/107 contribute to HBx-induced hepatocellular carcinoma progression through suppression of maspin.
Oncotarget. 2015; 6(28):25962-74 [PubMed] Article available free on PMC after 01/05/2017 Related Publications
Maspin suppresses tumor progression by promoting cell adhesion and apoptosis and by inhibiting cell motility. However, its role in tumorigenesis of hepatocellular carcinoma (HCC) remains unclear. The gene regulation of maspin and its relationship with HCC patient prognosis were investigated in this study. Maspin expression was specifically reduced in HBV-associated patients and correlated with their poor prognosis. Maspin downregulation in HCC cells was induced by HBx to promote their motility and resistance to anoikis and chemotherapy. HBx-dependent induction of microRNA-7, -107, and -21 was further demonstrated to directly target maspin mRNA, leading to its protein downregulation. Higher expressions of these microRNAs also correlated with maspin downregulation in HBV-associated patients, and were associated with their poor overall survival. These data not only provided new insights into the molecular mechanisms of maspin deficiency by HBx, but also indicated that downregulation of maspin by microRNAs confers HBx-mediated aggressiveness and chemoresistance in HCC.

Zhang JJ, Wang CY, Hua L, et al.
miR-107 promotes hepatocellular carcinoma cell proliferation by targeting Axin2.
Int J Clin Exp Pathol. 2015; 8(5):5168-74 [PubMed] Article available free on PMC after 01/05/2017 Related Publications
BACKGROUND: A large number of studies demonstrated that microRNAs play important roles in the progression and development of human cancers. However, the expression level of miR-107 and its biological function in hepatocellular carcinoma (HCC) remains unclear.
METHOD: Quantitative real-time PCR (qRT-PCR) was used to evaluate the expression level of miR-107 in HCC tissues and cell lines. Then, we explored the function of miR-107 to determine its potential roles on HCC cell proliferation in vitro. Luciferase reporter assay was used to confirm the target gene of miR-107, and the results were validated in cell lines.
RESULTS: miR-107 was significantly up-regulated in HCC tissues and cell lines. The enforced expression of miR-107 was able to promote cell proliferation in HepG2 cells. At the molecular level, our results suggested that expression of Axin2 was negatively regulated by miR-107.
CONCLUSION: Our observations suggested that miR-107 could promote HCC cells proliferation via targeting Axin2 and might represent a potential therapeutic target for HCC.

Xu C, Xie S, Song C, et al.
Lin28 Mediates Cancer Chemotherapy Resistance via Regulation of miRNA Signaling.
Hepatogastroenterology. 2014; 61(132):1138-41 [PubMed] Related Publications
Chemotherapy resistance is one of the major obstacles limiting the success of cancer drug treatment. Among the mechanisms of resistance to chemotherapy treatment, there are those closely related to P-Glycoprotein, multidrug resistance-related protein, glutathione S-transferase pi and topoisomerase-II. Lin28 is a highly conserved RNA-binding protein, it consists of a cold shock domain and retroviral-type (CCHC) zinc finger motifs. In previous preclinical and clinical studies, positive Lin28 expression in cancer cells was correlated with decreased sensitivity to chemotherapy. And Lin28 could mediate cancer chemotherapy resistance via regulation of miR107 and Let-7 MiRNA. This article reviews current knowledge on predictive value of Lin28 in response to chemotherapy. Better understanding of its role may facilitate patient's selection of therapeutic regimen and lead to optimal clinical outcome.

Chen L, Li ZY, Xu SY, et al.
Upregulation of miR-107 Inhibits Glioma Angiogenesis and VEGF Expression.
Cell Mol Neurobiol. 2016; 36(1):113-20 [PubMed] Related Publications
MicroRNAs can function as oncogenes or tumor suppressors in glioma. Previously, we showed that miR-107 inhibits glioma cell proliferation, migration, and invasion. Since tumor growth and invasion are closely related to angiogenesis, we further examined the role of miR-107 in glioma angiogenesis. In a co-culture of glioma cells and human brain microvascular endothelial cells (HBMVEC), overexpression of miR-107 in glioma cells led to the inhibition of HBMVEC proliferation, migration, and tube formation ability. ELISA, RT-PCR, and western blot assays revealed that upregulation of miR-107 in glioma cells inhibits VEGF expression. Our findings collectively support the critical involvement of miR-107 in glioma cell angiogenesis and highlight its potential as a therapeutic target for glioma.

Stückrath I, Rack B, Janni W, et al.
Aberrant plasma levels of circulating miR-16, miR-107, miR-130a and miR-146a are associated with lymph node metastasis and receptor status of breast cancer patients.
Oncotarget. 2015; 6(15):13387-401 [PubMed] Article available free on PMC after 01/05/2017 Related Publications
Within the multicenter SUCCESS trial, we investigated the association of plasma microRNAs with different subtypes of invasive breast cancer.Six miRs (miR-16, miR-27a, miR-107, miR-130a, miR-132 and miR-146a) were selected from microarray profiling and further validated in plasma of 111 breast cancer patients before and after chemotherapy and 46 healthy women by quantitative real-time PCR.Plasma levels of miR-16 (p = 0.0001), miR-27a (p = 0.039) and miR-132 (p = 0.020) were higher in breast cancer patients before chemotherapy than healthy women. With the exception of miR-16, the increased levels of miR-27a (p = 0.035) and miR-132 (p = 0.025) decreased after chemotherapy to those observed in healthy women. Levels of miR-16 (p = 0.019), miR-107 (p = 0.036), miR-130a (p = 0.027) and miR-146a (p = 0.047) were different between lymph node -positive and -negative patients, while the levels of miR-130a (p = 0.001) and miR-146a (p = 0.025) also differed between HER2-positive and -negative status. Estrogen-receptor negative tumors displayed higher concentrations of circulating miR-107 than their counterparts (p = 0.035). However, overexpression of miR-107 in MCF-7 cells did not downregulate estrogen receptor protein. Altered expression levels of miR-107 influenced the migration and invasion behavior of MCF-7 and MDA-MB-231 cells.Our data indicate differential concentrations of plasma miR-16, miR-107, miR-130a and miR-146a in different breast cancer subtypes, suggesting a potential role of these miRs in breast cancer biology and tumor progression.

Zhang L, Ma P, Sun LM, et al.
MiR-107 down-regulates SIAH1 expression in human breast cancer cells and silencing of miR-107 inhibits tumor growth in a nude mouse model of triple-negative breast cancer.
Mol Carcinog. 2016; 55(5):768-77 [PubMed] Related Publications
We have reported that SIAH1 is down-regulated and associated with apoptosis and invasion in human breast cancer. However, the molecular mechanisms leading to SIAH1 down-regulation remain to be elucidated. Here, we demonstrated that miR-107 directly down-regulates SIAH1 expression in human breast cancer cells. Over- expression of miR-107 reduced SIAH1 expression, promoted human breast cancer cell proliferation, colony formation, migration and invasion, and inhibited apoptosis. On the contrary, silencing of miR-107 increased SIAH1 expression and inhibited the tumor growth of MDA-MB-231 cells, a kind of triple-negative breast cancer (TNBC) cells, in vitro and in vivo. Our results reveal that miR-107 is an upstream regulator for SIAH1 down-regulation in human breast cancer cells and miR-107 provides a potential effective target for the treatment of TNBC.

Zhang M, Wang X, Li W, Cui Y
miR-107 and miR-25 simultaneously target LATS2 and regulate proliferation and invasion of gastric adenocarcinoma (GAC) cells.
Biochem Biophys Res Commun. 2015; 460(3):806-12 [PubMed] Related Publications
Although a series of oncogenes and tumor suppressors were identified in the pathological development of gastric adenocarcinoma (GAC), the underlying molecule mechanism were still not fully understood. The current study explored the expression profile of miR-107 and miR-25 in GAC patients and their downstream regulative network. qRT-PCR analysis was performed to quantify the expression of these two miRNAs in serum samples from both patients and healthy controls. Dual luciferase assay was conducted to verify their putative bindings with LATS2. MTT assay, cell cycle assay and transwell assay were performed to explore how miR-107 and miR-25 regulate proliferation and invasion of gastric cancer cells. Findings of this study demonstrated that total miR-107 or miR-25 expression might be overexpressed in gastric cancer patients and they can simultaneously and synchronically regulate LATS2 expression, thereby affecting gastric cancer cell growth and invasion. Therefore, the miR-25/miR-107-LATS2 axis might play an important role in proliferation and invasion of the gastric cancer cells.

Wang S, Lv C, Jin H, et al.
A common genetic variation in the promoter of miR-107 is associated with gastric adenocarcinoma susceptibility and survival.
Mutat Res. 2014; 769:35-41 [PubMed] Related Publications
BACKGROUND: Global miRNA expression profile has been widely used to characterize human cancers. It is well established that genetic variants in miRNAs can modulate miRNA biogenesis and disease risk.
METHODS: Genome-wide miRNA microarray was employed for assessment of miRNA expression profile of gastric adenocarcinoma (GAC). The variants of significantly dysregulated miRNA were genotyped in test (715 cases and 804 controls) and validation (940 cases and 1050 controls) subject sets.
RESULTS: MiRNA microarray revealed that 12 miRNAs including miR-107 significantly dysregulated in GAC tissues. The sequencing of the promoter of miR-107 identified 3 SNPs (rs11185777, rs78591545, and rs2296616) with minor allele frequency (MAF)>5%. Analyzing their association with GAC risk and prognosis revealed that the C allele of rs2296616 (T>C) was significantly associated with the decreased risk of GAC among the test, validation and combined sets (TC/CC vs. TT, adjusted OR=0.39, 95% CI=0.31-0.49 for the combined set). However, the C allele was related to an unfavorable prognosis of Cardia GAC (CGAC) (adjusted HR=1.49, 95% CI=1.01-2.20). In vivo evidence showed that the individuals with the rs2296616C allele had lower miR-107 expression compared with the homozygous T allele carriers.
CONCLUSION: miR-107 is dysregulated in GAC pathogenesis and the SNP rs2296616 may play a role in the process.

Tao J, Ji J, Li X, et al.
Distinct anti-oncogenic effect of various microRNAs in different mouse models of liver cancer.
Oncotarget. 2015; 6(9):6977-88 [PubMed] Article available free on PMC after 01/05/2017 Related Publications
Deregulation of microRNAs (miRNAs) is a typical feature of human hepatocellular carcinoma (HCC). However, the in vivo relevance of miRNAs along hepatocarcinogenesis remains largely unknown. Here, we show that liver tumors induced in mice by c-Myc overexpression or AKT/Ras co-expression exhibit distinct miRNA expression profiles. Among the downregulated miRNAs, eight (miR-101, miR-107, miR-122, miR-29, miR-365, miR-375, miR-378, and miR-802) were selected and their tumor suppressor activity was determined by overexpressing each of them together with c-Myc or AKT/Ras oncogenes in mouse livers via hydrodynamic transfection. The tumor suppressor activity of these microRNAs was extremely heterogeneous in c-Myc and AKT/Ras mice: while miR-378 had no tumor suppressor activity, miR-107, mir-122, miR-29, miR-365 and miR-802 exhibited weak to moderate tumor suppressor potential. Noticeably, miR-375 showed limited antineoplastic activity against c-Myc driven tumorigenesis, whereas it strongly inhibited AKT/Ras induced hepatocarcinogenesis. Furthermore, miR-101 significantly suppressed both c-Myc and AKT/Ras liver tumor development. Altogether, the present data demonstrate that different oncogenes induce distinct miRNA patterns, whose modulation differently affects hepatocarcinogenesis depending on the driving oncogenes. Finally, our findings support a strong tumor suppressor activity of miR-101 in liver cancer models regardless of the driver oncogenes involved, thus representing a promising therapeutic target in human HCC.

Song N, Ma X, Li H, et al.
microRNA-107 functions as a candidate tumor suppressor gene in renal clear cell carcinoma involving multiple genes.
Urol Oncol. 2015; 33(5):205.e1-11 [PubMed] Related Publications
BACKGROUND: MicroRNAs (miRNAs) are small RNAs with oncogenic and tumor-suppressing functions in cancer. miRNAs not only regulate various target genes but also participate in vital signaling pathways.
METHODS AND RESULTS: The tumor-suppressing function of miRNA-107 (miR-107) was confirmed in clear cell renal cell carcinoma in 52 paired clinical specimens and renal cell carcinoma cell lines. Significant correlations were noted between clinical features and miR-107 expression level. Lentiviral vector and biosynthesis mimics were used to overexpress pre-miR-107 or mimicked miR-107 to investigate further the tumorigenesis of miR-107 in vivo and in vitro. Cell proliferation and invasiveness were inhibited in the 786-O cell line after miR-107 was delivered. High miR-107 level expression can apparently induce cell cycle arrest at the G2/M phase and retard tumor growth in nude mice. In addition, eukaryotic translation initiation factor 5 was found to be a direct target of miR-107 and exhibited an inverse relationship with miR-107. It was seen that p53 and VHL genes, which are implicated in renal tumors, were associated with miR-107.
CONCLUSION: In summary, our results showed that miR-107 can inhibit cell proliferation and invasiveness of renal cell carcinoma. Furthermore, this study may provide a potential therapeutic regimen for clear cell renal cell carcinoma treatment.

Ji Y, Wei Y, Wang J, et al.
Decreased expression of microRNA-107 predicts poorer prognosis in glioma.
Tumour Biol. 2015; 36(6):4461-6 [PubMed] Related Publications
The expression level of microRNA-107 (miR-107) has been proved to be decreased in many human malignant cancers. Especially in glioma, accumulating evidence indicates that miR-107 may play important parts in cell proliferation, apoptosis, and invasion in glioma. However, its clinical significance in glioma has not been investigated. This study aims at investigating the relationship between miR-107 expression level and clinical significance and analyzing its value of miR-107 in valuing the prognosis of glioma patients. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to measure the expression of miR-107 in 80 glioma and 17 normal brain tissues. The results showed the miR-107 expression level in glioma tissues was significantly lower than those in normal brain tissues (p < 0.001). The decreased expression of miR-107 in glioma was positively associated with high WHO grade (p < 0.001), low Karnofsky performance score (KPS) (p < 0.001), and large tumor size (p < 0.001) and had a significant impact on overall survival (OS) (p < 0.001) and progression-free survival (PFS) (p < 0.001) according to Kaplan-Meier survival with log-rank test. Finally, Cox regression analyses showed that low miR-107 expression (p < 0.001) might be an independent prognostic parameter to predict poor prognosis. In conclusion, it is the first data to prove that expression level of miR-107 may be a novel and valuable prognostic factor in glioma.

Kleivi Sahlberg K, Bottai G, Naume B, et al.
A serum microRNA signature predicts tumor relapse and survival in triple-negative breast cancer patients.
Clin Cancer Res. 2015; 21(5):1207-14 [PubMed] Related Publications
PURPOSE: Triple-negative breast cancers (TNBC) are associated with high risk of early tumor recurrence and poor outcome. Common prognostic biomarkers give very restricted predictive information of tumor recurrences in TNBC. Human serum contains stably expressed microRNAs (miRNAs), which have been discovered to predict prognosis in patients with cancer. The purpose of this study was to identify circulating biomarkers able to predict clinical outcome in TNBC.
EXPERIMENTAL DESIGN: We performed genome-wide serum miRNA expression and real-time PCR analyses to investigate the ability of miRNAs in predicting tumor relapse in serum samples from 60 primary TNBC. Patients were divided into training and testing cohorts.
RESULTS: By Cox regression analysis, we identified a four-miRNA signature (miR-18b, miR-103, miR-107, and miR-652) that predicted tumor relapse and overall survival. This miRNA signature was further validated in an independent cohort of 70 TNBC. A high-risk signature score was developed and significantly associated with tumor recurrence and reduced survival. Multivariate Cox regression models indicated that the risk score based on the four-miRNA signature was an independent prognostic classifier of patients with TNBC.
CONCLUSIONS: This signature may serve as a minimally invasive predictor of tumor relapse and overall survival for patients with TNBC. This prediction model may ultimately lead to better treatment options for patients with TNBC.

Zhang Z, Zhang L, Yin ZY, et al.
miR-107 regulates cisplatin chemosensitivity of A549 non small cell lung cancer cell line by targeting cyclin dependent kinase 8.
Int J Clin Exp Pathol. 2014; 7(10):7236-41 [PubMed] Article available free on PMC after 01/05/2017 Related Publications
Previous studies demonstrated that the acquired drug resistance of non-small cell lung cancer (NSCLC) was related to deregulation of miRNAs. However, the effects of miR-107 and the mechanism through which miR-107 affects the cisplatin chemoresistance in NSCLC have not been reported. TaqMan RT-PCR or Western blot assay was performed to detect the expression of mature miR-107 and cyclin dependent kinase 8 (CDK8) protein. The viabilities of treated cells were analyzed using MTT assay. We found that the expression level of miR-107 in A549 cells was significantly lower than that in normal human bronchial epithelial cells (0.45 ± 0.26 vs. 1.00 ± 0.29, P = 0.032). The MTT assay showed that the A549 cells transfected with miR-107 mimics were significantly more sensitive to the therapy of cisplatin than control cells. A549 cells transfected with miR-107 mimics showed a decreased CDK8 protein expression. Downregulation of CDK8 expression by siRNAs, A549 cells became more sensitive to the therapy of cisplatin. In addition, the enhanced growth-inhibitory effect by the miR-107 mimic transfection was enhanced after the addition of CDK8 siRNA. In conclusion, the present study provides the first evidence that miR-107 plays a key role in cisplatin resistance by targeting the CDK8 protein in NSCLC cell lines, suggesting that miR-107 can be used to predict a patient's response to chemotherapy as well as serve as a novel potential maker for NSCLC therapy.

Zhou C, Li G, Zhou J, et al.
miR-107 activates ATR/Chk1 pathway and suppress cervical cancer invasion by targeting MCL1.
PLoS One. 2014; 9(11):e111860 [PubMed] Article available free on PMC after 01/05/2017 Related Publications
MicroRNAs (miRNAs) are a class of single-stranded, non-coding RNAs of about 22 nucleotides in length. Increasing evidence implicates miRNAs may function as oncogenes or tumor suppressors. Here we showed that miR-107 directly targeted MCL1 and activated ATR/Chk1 pathway to inhibit proliferation, migration and invasiveness of cervical cancer cells. Moreover, we found that MCL1 was frequently up-regulated in cervical cancer, and knockdown of MCL1 markedly inhibited cancer cell proliferation, migration and invasion, whereas ectopic expression of MCL1 significantly enhances these properties. The restoration of MCL1 expression can counteract the effect of miR-107 on the cancer cells. Together, miR-107 is a new regulator of MCL1, and both miR-107 and MCL1 play important roles in the pathogenesis of cervical cancer. We have therefore identified a mechanism for ATR/Chk1 pathway which involves an increase in miR-107 leading to a decrease in MCL1. Correspondingly, our results revealed that miR-107 affected ATR/Chk1 signalling and gene expression, and implicated miR-107 as a therapeutic target in human cervical cancer. We also demonstrated that taxol attenuated migration and invasion in cervical cancer cells by activating the miR-107, in which miR-107 play an important role in regulating the expression of MCL1. Elucidation of this discovered MCL1 was directly regulated by miR-107 will greatly enhance our understanding of the mechanisms responsible for cervical cancer and will provide an additional arm for the development of anticancer therapies.

Ruan J, Liu X, Xiong X, et al.
miR‑107 promotes the erythroid differentiation of leukemia cells via the downregulation of Cacna2d1.
Mol Med Rep. 2015; 11(2):1334-9 [PubMed] Related Publications
microRNAs (miRNAs) have been reported to be involved in various human diseases. They may have uses in diagnosis and as therapeutic targets, thus the discovery of novel miRNAs has the potential to provide clinical tools or shed light on novel mechanisms. In the current study, miR‑107 was revealed to be downregulated in chronic myeloid leukemia cells. Overexpression of miR‑107 in K562 and KCL‑22 chronic myeloid leukemia cells promotes erythroid differentiation, while having no effect on cell proliferation. Further bioinformatics predicted that one target of miR‑107 may be Cacna2d1, a calcium channel protein. A luciferase reporter assay and quantitative polymerase chain reaction were utilized to confirm that Cacna2d1 is a target molecule of miR-107. The effect of miR‑107 on K562 and KCL‑22 cells was mediated through the downregulation of Cacna2d1, as rescued expression of Cacna2d1 reversed the effects of miR‑107. In summary, the current study identified a novel miRNA that is involved in chronic myeloid leukemia cell erythroid differentiation and the associated mechanisms, making it a potential therapeutic target in the treatment of chronic myeloid leukemia.

Akçakaya P, Caramuta S, Åhlen J, et al.
microRNA expression signatures of gastrointestinal stromal tumours: associations with imatinib resistance and patient outcome.
Br J Cancer. 2014; 111(11):2091-102 [PubMed] Article available free on PMC after 01/05/2017 Related Publications
BACKGROUND: Gastrointestinal stromal tumour (GIST) is mainly initialised by receptor tyrosine kinase gene mutations. Although the tyrosine kinase inhibitor imatinib mesylate considerably improved the outcome of patients, imatinib resistance still remains a major therapeutic challenge in GIST therapy. Herein we evaluated the clinical impact of microRNAs in imatinib-treated GISTs.
METHODS: The expression levels of microRNAs were quantified using microarray and RT-qPCR in GIST specimens from patients treated with neoadjuvant imatinib. The functional roles of miR-125a-5p and PTPN18 were evaluated in GIST cells. PTPN18 expression was quantified by western blotting in GIST samples.
RESULTS: We showed that overexpression levels of miR-125a-5p and miR-107 were associated with imatinib resistance in GIST specimens. Functionally, miR-125a-5p expression modulated imatinib sensitivity in GIST882 cells with a homozygous KIT mutation but not in GIST48 cells with double KIT mutations. Overexpression of miR-125a-5p suppressed PTPN18 expression, and silencing of PTPN18 expression increased cell viability in GIST882 cells upon imatinib treatment. PTPN18 protein levels were significantly lower in the imatinib-resistant GISTs and inversely correlated with miR-125a-5p. Furthermore, several microRNAs were significantly associated with metastasis, KIT mutational status and survival.
CONCLUSIONS: Our findings highlight a novel functional role of miR-125a-5p on imatinib response through PTPN18 regulation in GIST.

Molina-Pinelo S, Carnero A, Rivera F, et al.
MiR-107 and miR-99a-3p predict chemotherapy response in patients with advanced colorectal cancer.
BMC Cancer. 2014; 14:656 [PubMed] Article available free on PMC after 01/05/2017 Related Publications
BACKGROUND: MicroRNAs (miRNAs) are involved in numerous biological and pathological processes including colorectal cancer (CRC). The aim of our study was to evaluate the ability of miRNA expression patterns to predict chemotherapy response in a cohort of 78 patients with metastatic CRC (mCRC).
METHODS: We examined expression levels of 667 miRNAs in the training cohort and evaluated their potential association with relevant clinical endpoints. We identified a miRNA profile that was analysed by RT-qPCR in an independent cohort. For a set of selected miRNAs, bioinformatic target predictions and pathway analysis were also performed.
RESULTS: Eight miRNAs (let-7 g*, miR-107, miR-299-5p, miR-337-5p, miR-370, miR-505*, miR-889 and miR-99a-3p) were significant predictors of response to chemotherapy in the training cohort. In addition, overexpression of miR-107, miR-337-5p and miR-99a-3p, and underexpression of miR-889, were also significantly associated with improved progression-free and/or overall survival. MicroRNA-107 and miR-99a-3p were further validated in an independent cohort as predictive markers for chemotherapy response. In addition, an inverse correlation was confirmed in our study population between miR-107 levels and mRNA expression of several potential target genes (CCND1, DICER1, DROSHA and NFKB1).
CONCLUSIONS: MiR-107 and miR-99a-3p were validated as predictors of response to standard fluoropyrimidine-based chemotherapy in patients with mCRC.

Song YQ, Ma XH, Ma GL, et al.
MicroRNA-107 promotes proliferation of gastric cancer cells by targeting cyclin dependent kinase 8.
Diagn Pathol. 2014; 9:164 [PubMed] Article available free on PMC after 01/05/2017 Related Publications
BACKGROUND: The biological processes and molecular mechanisms underlying miR-107 remain unclear in gastric cancer(GC). In this study, we aimed to investigate the expression, biological functions and mechanisms of miR-107 in GC.
METHODS: Quantitative real-time RT-PCR was used to test miR-107 expression. MTT and colony formation assays were conducted to explore the potential function of miR-107 in human GC cell line SGC7901. The target gene was determined by bioinformatic algorithms, dual luciferase reporter assay, RT-PCR and Western blot.
RESULTS: Expression of miR-107 was significantly elevated in GC cell line than that in gastric epithelial cell line(p = 0.012). We found that miR-107 inhibitor transfection significantly decreased the proliferation of GC cell line, and clone formation rate of miR-107 inhibitor transfected group was significantly lower than that of control group. Luciferase assays using a reporter carrying a putative miR-107 target site in the 3'untranslated region (3'-UTR) of cyclin dependent kinase 8 (CDK8) revealed that miR-107 directly targets CDK8. The expression level of CDK8 mRNA and protein in miR-107 inhibitor transfected GC cell line was significantly decreased compared with control group.
CONCLUSION: Our findings indicate that miR-107 is upregulated in GC and affects the proliferation of GC cells, partially through the regulation of CDK8.
VIRTUAL SLIDES: The virtual slide(s) for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/13000_2014_164.

Zhong KZ, Chen WW, Hu XY, et al.
Clinicopathological and prognostic significance of microRNA-107 in human non small cell lung cancer.
Int J Clin Exp Pathol. 2014; 7(7):4545-51 [PubMed] Article available free on PMC after 01/05/2017 Related Publications
BACKGROUND: MicroRNAs (miRNAs) are small, non-coding RNAs which can function as oncogenes or tumor suppressor genes in human cancers. Researchers have found that the expression level of miR-107 was decreased in human non-small cell lung cancer (NSCLC) tissues and cell lines, however, its clinicopathological and prognostic significance in NSCLC has not been investigated.
METHODS: Quantitative real-time PCR (qRT-PCR) was used to analyze the expression of miR-107 in 137 pairs of fresh NSCLC and matched adjacent normal tissue specimens. The chi-square test and Fishers exact tests were used to examine the associations between miR-107 expression and the clinicopathological characters. The overall survival (OS) and progression-free survival (PFS) were analyzed by log-rank test, and survival curves were plotted according to Kaplan-Meier.
RESULTS: The expression level of miR-107 was significantly lower in tumor tissues than that in corresponding noncancerous tissues (0.4676 ± 0.2078 vs. 1.000 ± 0.3953, P<0.001). Low expression of miR-107 was found to significantly correlate with TNM stage (p=0.001), regional lymph node involvement (p=0.04), and tumor differentiation (p=0.003). Kaplan-Meier analysis with the log-rank test indicated that low miR-107 expression had a significant impact on OS (35.2% vs. 69.3%; P=0.008) and PFS (30.0% vs. 56.2%; P=0.029). In a multivariate Cox model, we found that miR-107 expression was an independent poor prognostic factor for both 5-year OS (HR=2.57, 95% CI: 1.88-10.28; P=0.007) and 5-year PFS (HR=3.08, 95% CI: 2.01-8.92; P=0.003).
CONCLUSION: The expression of miR-107 was decreased in NSCLC. Low expression of miR-107 was significantly associated with tumor progression and decreased survival in patients with NSCLC, indicating that miR-107 may serve as a novel prognostic marker in NSCLC.

Kodahl AR, Zeuthen P, Binder H, et al.
Alterations in circulating miRNA levels following early-stage estrogen receptor-positive breast cancer resection in post-menopausal women.
PLoS One. 2014; 9(7):e101950 [PubMed] Article available free on PMC after 01/05/2017 Related Publications
INTRODUCTION: Circulating microRNAs (miRNAs) exhibit remarkable stability and may serve as biomarkers in several clinical cancer settings. The aim of this study was to investigate changes in the levels of specific circulating miRNA following breast cancer surgery and evaluate whether these alterations were also observed in an independent data set.
METHODS: Global miRNA analysis was performed on prospectively collected serum samples from 24 post-menopausal women with estrogen receptor-positive early-stage breast cancer before surgery and 3 weeks after tumor resection using global LNA-based quantitative real-time PCR (qPCR).
RESULTS: Numbers of specific miRNAs detected in the samples ranged from 142 to 161, with 107 miRNAs detectable in all samples. After correction for multiple comparisons, 3 circulating miRNAs (miR-338-3p, miR-223 and miR-148a) exhibited significantly lower, and 1 miRNA (miR-107) higher levels in post-operative vs. pre-operative samples (p<0.05). No miRNAs were consistently undetectable in the post-operative samples compared to the pre-operative samples. Subsequently, our findings were compared to a dataset from a comparable patient population analyzed using similar study design and the same qPCR profiling platform, resulting in limited agreement.
CONCLUSIONS: A panel of 4 circulating miRNAs exhibited significantly altered levels following radical resection of primary ER+ breast cancers in post-menopausal women. These specific miRNAs may be involved in tumorigenesis and could potentially be used to monitor whether all cancer cells have been removed at surgery and/or, subsequently, whether the patients develop recurrence.

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