Locus Summary

Gene:MIR1297; microRNA 1297
Aliases: MIRN1297, mir-1297, hsa-mir-1297
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, HGNC, Ensembl, GeneCard, Gene
Source:NCBIAccessed: 31 August, 2019

Cancer Overview

Research Indicators

Publications Per Year (1994-2019)
Graph generated 31 August 2019 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 31 August, 2019 using data from PubMed, MeSH and CancerIndex

Specific Cancers (12)

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)MIR1297 Function in CancerEffect
lung (1)
-lung cancer (1)
TRIB2 (1)
inhibit cell proliferation (1)
tumor-suppressive (1)
head and neck (1)
-laryngeal squamous cell carcinoma (1)
PTEN (1)
promote cell proliferation (1)
promote cell migration (1)
promote tumorgenesis (1)
oncogenic (1)

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

Latest Publications: MIR1297 (cancer-related)

Chen Z, Zhang M, Qiao Y, et al.
MicroRNA-1297 contributes to the progression of human cervical carcinoma through PTEN.
Artif Cells Nanomed Biotechnol. 2018; 46(sup2):1120-1126 [PubMed] Related Publications
BACKGROUND: The human cervical carcinoma oncogenic mechanisms still remain elusive. Thus, we proposed to understand the biological role of a newly discovered therapeutic miRNA.
METHODS: MiR-1297 related to human cervical carcinoma was selected for this study. TaqMan qRT- PCR assay was used to profile miRNA, phosphatase and tensin homolog (PTEN) expression in randomly chosen tumour with non-tumour tissues, and the apoptosis factors expression. Cell proliferation was monitored by CCK-8 assay and colony formation assay. Apoptosis was determined by flow cytometry. Protein level was determined by western blotting. 3'UTR was performed to validate the direct binding sites of miR-1297 on PTEN. SPSS was used for statistical analyses.
RESULTS: MiR-1297 is repressed and PTEN activated in human cervical cancer tissues. After miR-1297 overexpression, HeLa cells had an increase in cell proliferation and decrease in apoptosis. PTEN expression is negatively correlation with miR-1297. PTEN silencing display the similar pattern as miRNA-1297 overexpression to inhibit HeLa cell growth and apoptosis in vitro.
CONCLUSIONS: Our data indicate that miR-1297 contribute to the human cervical carcinoma through PTEN. miR-1297 could be a reasonable miRNA for future studies.

Chen Z, Ma Y, Pan Y, et al.
MiR-1297 suppresses pancreatic cancer cell proliferation and metastasis by targeting MTDH.
Mol Cell Probes. 2018; 40:19-26 [PubMed] Related Publications
Dysregulation of miR-1297 has been detected in various human cancers, and miR-1297 can function as either an oncogene or tumor suppressor. However, the role of miR-1297 in pancreatic adenocarcinoma has not been previously reported. Here, we investigated miR-1297 expression in pancreatic cancer and the role it plays in the development and metastasis of pancreatic adenocarcinoma. In the present study, MiR-1297 and metadherin (MTDH) expression in pancreatic cancer tissue was detected using quantitative real-time PCR (qRT-PCR) and western blot methods. The CCK-8 assay and EdU incorporation assay were used to analyze the impact of miR-1297 and MTDH on cell proliferation. Flow cytometric and Hoechst 33342 staining methods were used to explore how miR-1297 and MTDH affect cell apoptosis. The Transwell assay and scratch wound healing assay were used to analyze cell migration and invasion capabilities. The dual-luciferase assay was used to confirm that miR-1297 targets MTDH. Here, we found that miR-1297 expression was decreased in pancreatic adenocarcinoma tissues, while MTDH expression was increased in those tissues. Furthermore, western blot and dual-luciferase assay results confirmed that MTDH was a direct target of miR-1297. Additionally, overexpression of miR-1297 or knockdown of MTDH suppressed BxPC-3 and PANC-1 cell proliferation, and upregulation of miR-1297 or suppression of MTDH promoted BxPC-3 and PANC-1 cell apoptosis. Finally, BxPC-3 and PANC-1 cell migration and invasion abilities were suppressed by either overexpression of miR-1297 or downregulation of MTHD. In conclusion, our results suggest that miR-1297 inhibits the growth and metastasis of pancreatic adenocarcinoma by downregulating MTDH expression, and the miR-1297/MTDH pathway is a potential target for treating pancreatic adenocarcinoma.

Gao W, Cao Y, Guo P, et al.
Downregulation of MiR-1297 predicts poor prognosis and enhances gastric cancer cell growth by targeting CREB1.
Biomed Pharmacother. 2018; 105:413-419 [PubMed] Related Publications
Dysregulation of mircoRNAs (miRs) that act as tumor suppressors or oncogenes is participated in tumorigenesis and progression. The aim of the study is to investigate the role and mechanism of miR-1297 in gastric cancer (GC). Here, we demonstrated that miR-1297 expression was significantly lower in GC tissue samples compared to adjacent normal tissue samples in 62 cases GC patients. Lower miR-1297 expression positively associated with larger tumor size, lymph node metastasis, advanced TNM stage and poor survival time of patients. Upregulation of miR-1297 significantly inhibited cell proliferation and cell colony forming abilities in vitro. However, downregulation of miR-1297 can cause the reverse biological function changes. In vivo, miR-1297 overexpression suppressed tumor growth. Luciferase reporter assay showed that CREB1 was a direct target of miR-1297 in GC. MiR-1297 inhibited the expression of CREB1 by targeting the 3'UTR of CREB1. Additionally, we demonstrated that CREB1 overexpression rescued the effects on GC cell growth induced by miR-1297. Therefore, these results indicated that miR-1297 might be a prognostic predictor for GC and potential target of GC treatment.

Guo T, Wang H, Liu P, et al.
SNHG6 Acts as a Genome-Wide Hypomethylation Trigger via Coupling of miR-1297-Mediated S-Adenosylmethionine-Dependent Positive Feedback Loops.
Cancer Res. 2018; 78(14):3849-3864 [PubMed] Related Publications
Aberrant genome-wide hypomethylation and long noncoding RNA (lncRNA) dysregulation are associated with hepatocarcinogenesis. However, whether a relationship between the two exists remains largely unknown. S-adenosylmethionine (SAMe)-dependent methylation is a critical factor in genomic methylation. We previously found that SNHG6 lncRNA acted as an oncogene in hepatocarcinogenesis and could be considered a potential prognostic indicator for hepatocellular carcinoma (HCC). Here we verify that SNHG6 leads to genome-wide hypomethylation in hepatoma cells and that SNHG6 negatively correlates with the steady-state SAMe concentration

Wang Z, He S, Guo P, et al.
MicroRNA-1297 inhibits metastasis and epithelial-mesenchymal transition by targeting AEG-1 in cervical cancer.
Oncol Rep. 2017; 38(5):3121-3129 [PubMed] Related Publications
Accumulating evidence has demonstrated that aberrant miRNAs contribute to cervical cancer (CC) development and progression. However, the roles of various miRNAs in CC remain to be determined. In the present study, we confirmed that a decreased miR-1297 expression was present in CC tissues and cell lines. Our clinical analysis revealed that the downregulated miR-1297 expression was significantly correlated with poor prognostic features including lymph node metastasis and lymphovascular space invasion. Moreover, we confirmed that miR-1297 was a novel independent prognostic marker for predicting the 5-year survival of CC patients. The ectopic overexpression of miR-1297 inhibited cell migration, invasion and EMT progression, while downregulated miR-1297 reversed these effects. In addition, miR-1297 regulated AEG-1 by directly binding to its 3'-UTR. In clinical samples of CC, miR-1297 was inversely correlated with AEG-1, which was upregulated in CC. Alteration of AEG-1 expression at least partially abolished the migration, invasion and EMT progression effects of miR-1297 on CC cells. In conclusion, our results indicated that miR-1297 functioned as a tumor suppressor gene in regulating the EMT and metastasis of CC via targeting of AEG-1, and may represent a novel potential therapeutic target and prognostic marker for CC.

Wang Y, Xue J, Kuang H, et al.
microRNA-1297 Inhibits the Growth and Metastasis of Colorectal Cancer by Suppressing Cyclin D2 Expression.
DNA Cell Biol. 2017; 36(11):991-999 [PubMed] Related Publications
microRNAs (miR) can potentially be used for categorizing the various subtypes of colorectal cancer (CRC) and predicting a patient's response to treatment with traditional anti-CRC therapies. We investigated how miR-1297 and its potential target molecule cyclin D2 (CCND2) might affect the progression of CRC. Thirty-two pairs of CRC specimens and corresponding samples of para-tumor tissue were collected and examined for their levels of miR-1297 and CCND2 expression. We also examined miR-1297 and CCND2 expression in cultured SW480 cells. The effects of modulated levels of miR-1297 and CCND2 on cell viability, anchorage-independent growth ability, proliferation, apoptosis, cell cycle distribution, migration, and invasion were detected using specific techniques. The possible regulatory effect of miR-1297 on CCND2 was investigated using dual luciferase assays. Our results showed that miR-1297 expression was downregulated in clinical CRC specimens, and such downregulation was associated with upregulated levels of CCND2 expression. Upregulation of miR-1297 and downregulation of CCND2 reduced the proliferation and metastasis potential of SW480 cells, but did not affect the apoptotic process. In addition, miR-1297 regulated CCND2 function by directly binding to the promoter sequence of the CCND2 gene, which would block CCND2-related signaling at the transcription level. Our findings validate the anti-CRC function of miR-1297 and pro-CRC function of CCND2. Our findings may assist in developing miR-based therapies against CRC.

Bu W, Luo T
miR-1297 Promotes Cell Proliferation of Non-Small Cell Lung Cancer Cells: Involving in PTEN/Akt/Skp2 Signaling Pathway.
DNA Cell Biol. 2017; 36(11):976-982 [PubMed] Related Publications
Phosphatase and tensin homolog deleted on chromosome ten (PTEN) is a lipid and protein phosphatase and possesses an antitumor effect in lung cancers. miRNAs are reportedly abnormally expressed in human lung cancers. However, whether miRNA contributes to PTEN expression in non-small cell lung cancers (NSCLCs) has not been clearly clarified. In the present study, we found that miR-1297 probably binds with 3'UTR sequence of PTEN and negatively regulated the levels of PTEN in NSCLC cells. First, the expression levels of PTEN and Skp2 were detected by western blotting in NSCLC specimens and paired normal tissue specimens. The results showed that decreased levels of PTEN were detected in NSCLC tissues, compared with paired control tissues (**p < 0.01). The expression levels of PTEN were conversely correlated with the levels of Skp2 in clinical NSCLC specimens and NSCLC cell line. Transfection with miR-1297 mimic significantly promoted cell viability of A549 cells and NCI-H460 cells by downregulating the level of PTEN and upregulating the expression of Skp2. Interestingly, knockdown of Skp2 did not affect the expression of PTEN in A549 cells. Thus, miR-1297 might work as an oncogene by regulating PTEN/Akt/Skp2 signaling pathway in NSCLC cells. PTEN and Skp2 might be the potential targets in the clinical therapy of lung cancers.

Liu C, Liu Z, Li X, et al.
MicroRNA-1297 contributes to tumor growth of human breast cancer by targeting PTEN/PI3K/AKT signaling.
Oncol Rep. 2017; 38(4):2435-2443 [PubMed] Related Publications
Increasing evidence confirms that aberrant miRNA expression contributes to breast cancer (BC) development and progression. However, the roles of different miRNAs in BC remain to be explored. In the present study, we demonstrated that miR-1297 expression was increased in BC tissues and cell lines. Our clinical analysis revealed that the upregulated miR-1297 expression was significantly correlated with poor prognostic features including advanced TNM stage and larger tumor size. Moreover, we found that miR-1297 was a novel independent prognostic marker for predicting 5-year survival of BC patients. The ectopic overexpression of miR-1297 promoted cell proliferation, cell cycle progression and inhibited apoptosis while miR-1297 knockdown reversed the effect. In addition, miR-1297 modulated PTEN by directly binding to its 3'-UTR, resulting in activation of AKT signaling. In clinical samples of BC, miR-1297 inversely correlated with PTEN, which was downregulated in BC. Alternation of PTEN expression or AKT inhibitor at least partially abolished the biological effects of miR-1297 on BC cells. In conclusion, our results indicated that miR-1297 functioned as an oncogene in regulating the proliferation, cell cycle and apoptosis of BC via targeting PTEN/PI3K/AKT signaling, and may represent a novel potential therapeutic target and prognostic marker for BC.

Landero-Huerta DA, Vigueras-Villasenor RM, Yokoyama-Rebollar E, et al.
Epigenetic and risk factors of testicular germ cell tumors: a brief review.
Front Biosci (Landmark Ed). 2017; 22:1073-1098 [PubMed] Related Publications
Testicular germ cell cancer (TGCT) is the most common malignancy among young adult males, which has become important due to its increased incidence and mortality in the population worldwide. The etiology is multifactorial. Recent studies have shown some associations between the development of isolated TGCT and certain risk factors, such as exposure to endocrine disruptors, cryptorchidism, and family history of cancer, in order to identify the key pieces in carcinogenesis. Some of the most important findings in recent years is the association of different genes, such as

Sun M, Nie F, Wang Y, et al.
LncRNA HOXA11-AS Promotes Proliferation and Invasion of Gastric Cancer by Scaffolding the Chromatin Modification Factors PRC2, LSD1, and DNMT1.
Cancer Res. 2016; 76(21):6299-6310 [PubMed] Related Publications
Long noncoding RNAs (lncRNA) have been implicated in human cancer but their mechanisms of action are mainly undocumented. In this study, we investigated lncRNA alterations that contribute to gastric cancer through an analysis of The Cancer Genome Atlas RNA sequencing data and other publicly available microarray data. Here we report the gastric cancer-associated lncRNA HOXA11-AS as a key regulator of gastric cancer development and progression. Patients with high HOXA11-AS expression had a shorter survival and poorer prognosis. In vitro and in vivo assays of HOXA11-AS alterations revealed a complex integrated phenotype affecting cell growth, migration, invasion, and apoptosis. Strikingly, high-throughput sequencing analysis after HOXA11-AS silencing highlighted alterations in cell proliferation and cell-cell adhesion pathways. Mechanistically, EZH2 along with the histone demethylase LSD1 or DNMT1 were recruited by HOXA11-AS, which functioned as a scaffold. HOXA11-AS also functioned as a molecular sponge for miR-1297, antagonizing its ability to repress EZH2 protein translation. In addition, we found that E2F1 was involved in HOXA11-AS activation in gastric cancer cells. Taken together, our findings support a model in which the EZH2/HOXA11-AS/LSD1 complex and HOXA11-AS/miR-1297/EZH2 cross-talk serve as critical effectors in gastric cancer tumorigenesis and progression, suggesting new therapeutic directions in gastric cancer. Cancer Res; 76(21); 6299-310. ©2016 AACR.

Liang X, Li H, Fu D, et al.
MicroRNA-1297 inhibits prostate cancer cell proliferation and invasion by targeting the AEG-1/Wnt signaling pathway.
Biochem Biophys Res Commun. 2016; 480(2):208-214 [PubMed] Related Publications
MicroRNAs (miRNAs) have been known to be implicated in tumorigenic programs. miR-1297 has been reported to be dysregulated and involved in cancer progression in many types of human cancers. However, the expression level and the role of miR-1297 in prostate cancer remain unclear. Herein, we aimed to investigate the potential role and molecular mechanism of miR-1297 in prostate cancer progression. We found that miR-1297 was significantly downregulated in human prostate cancer specimens as well as in several prostate cancer cell lines. In addition, functional experiments demonstrated that overexpression of miR-1297 remarkably inhibited prostate cancer cell proliferation and invasion whereas miR-1297 suppression significantly promoted prostate cancer cell proliferation and invasion. Bioinformatics analysis showed that the Astrocyte elevated gene-1 (AEG-1), a well-known oncogene, is a predicted target of miR-1297. Dual-luciferase reporter assay showed that miR-1297 was able to directly target the 3'-untranslated region of AEG-1. In addition, RT-qPCR and Western blot analysis showed that miR-1297 regulated the mRNA and protein expression levels of AEG-1. We also showed that miR-1297 was able to regulate the Wnt signaling pathway. Moreover, rescue assays indicated that AEG-1 contributed to miR-1297-endowed effects on cell proliferation and invasion as well as Wnt signaling pathway. Taken together, these findings suggest that miR-1297 inhibits prostate cancer proliferation and invasion by targeting AEG-1, thereby providing novel insight into understanding the pathogenesis of prostate cancer. Thus, miR-1297 may be a novel potential therapeutic candidate to treat prostate cancer.

Ju HQ, Lu YX, Chen DL, et al.
Redox Regulation of Stem-like Cells Though the CD44v-xCT Axis in Colorectal Cancer: Mechanisms and Therapeutic Implications.
Theranostics. 2016; 6(8):1160-75 [PubMed] Free Access to Full Article Related Publications
Colorectal cancer (CRC) is a common neoplastic disease and a frequent cause of death. Drug resistance is a major challenge to CRC treatment and stem-like side-population (SP) cells may play a key role in this resistance. Although it has been recognized that cancer stem cells may be affected by redox status, the underlying mechanisms for this effect and the roles of celllular redox adaptation and antioxidant capacity in CRC remain elusive. Our study shows that CRC SP cells are highly dependent on cellular GSH to maintain ROS levels below those of non-SP cells. Exposing CRC cells to H2O2 produced a significant decrease in the percentage of SP cells, which was rescued by adding N-acetylcysteine. Mechanistically, CD44v interacts with and stabilizes xCT and thereby promotes the uptake of cysteine for GSH synthesis and stimulates SP cell enrichment. Additionally, miR-1297 levels were inversely correlated with the expression of xCT; thus, reduced miR-1297 contributes to SP cell enrichment in CRC tumors, which results in tumor aggressiveness and poor clinical outcomes. Importantly, redox modification by PEITC significantly reduces CRC SP cells in vitro and impairs tumors growth in vivo. The combination of 5FU and PEITC led to synergistic cytotoxic effects against CRC cells in vitro and in vivo. Taken together, our data suggest that a GSH-mediated reduction in cellular ROS levels is an essential regulator of CRC SP cells mediated by the CD44v-xCT axis, and disrupting the redox status may eliminate the chemotherapy-resistant CRC SP cells with potentially significant benefits for cancer treatment.

Wang C, Li Q, Liu F, et al.
Serum miR-1297: a promising diagnostic biomarker in esophageal squamous cell carcinoma.
Biomarkers. 2016; 21(6):517-22 [PubMed] Related Publications
We aimed to value the diagnostic potential of serum miR-1297 in esophageal squamous cell cancer (ESCC). Its expression level was detected in 156 pairs of patients with ESCC and healthy volunteers using quantitative real-time polymerase chain reaction (qRT-PCR) method. It was statistically decreased in ESCC patients compared with healthy controls. AUC based on serum miR-1297 was 0.840 ± 0.035 in discovery group and 0.837 ± 0.034 in validation group. Further analysis on early-stage patients revealed that the AUC was 0.819 ± 0.053 in discovery group and 0.814 ± 0.044 in validation group. Its sensitivity and specificity were promising. In conclusion, serum miR-1297 can serve as an ideal indicator for the diagnosis of ESCC.

Liu Y, Liang H, Jiang X
MiR-1297 promotes apoptosis and inhibits the proliferation and invasion of hepatocellular carcinoma cells by targeting HMGA2.
Int J Mol Med. 2015; 36(5):1345-52 [PubMed] Related Publications
MicroRNAs (miRNAs) have recently emerged as important regulators of gene expression in various tissues. In particular, miRNAs have been identified as new therapeutic agents and biomarkers in cancer. The aim of the present study was to explore whether miR‑1297 has an anti‑cancer role in hepatocellular carcinoma cell lines and to explore its underlying mechanism. The proliferation, apoptosis and migration of hepatocellular carcinoma cells were evaluated by cell viability assay, TUNEL staining and a wound healing assay, respectively. Western blot analysis and reverse transcription polymerase chain reaction (RT‑PCR) were performed to determine the expression levels of proteins and mRNAs of high‑mobility group AT‑hook 2 (HMGA2) in hepatocellular carcinoma. The luciferase assay was employed to verify the inhibitory activity of miR‑1297 on the 3' untranslated region (3'UTR) of the HMGA2 gene. In the present study, overexpression of miR‑1297 significantly inhibited the proliferation of HepG2 and SMMC7721 cells. Forced expression of miR‑1297 also increased the apoptosis of HepG2 and SMMC7721. Furthermore, the migration of HepG2 and SMMC7721 was also clearly suppressed by miR‑1297 overexpression. All these effects can be abrogated by co‑transfection with miR‑1297 inhibitor‑AMO‑1297. The luciferase assay verified that miR‑1297 overexpression is able to inhibit the activity of luciferase reporter harboring the HMGA2 3'UTR, indicating HMGA2 as the target of miR‑1297. Although the HMGA2 level was not affected by miR‑1297, the HMGA2 protein was significantly inhibited by miR‑1297 overexpression. Collectively, miR‑1297 was revealed to regulate the proliferation, apoptosis and migration of hepatocellular carcinoma cells via acting on HMGA2. The finding provides a new target for the treatment of hepatocellular carcinoma.

Liu F, He Y, Shu R, Wang S
MicroRNA-1297 regulates hepatocellular carcinoma cell proliferation and apoptosis by targeting EZH2.
Int J Clin Exp Pathol. 2015; 8(5):4972-80 [PubMed] Free Access to Full Article Related Publications
In this study, we suggested the level of miR-1297 was downreguled in the human hepatocellular carcinoma compared to the normal cells. We demonstrate ectopic expression of miR-1297 could significantly suppress hepatocellular carcinoma cells proliferation and enhance the cell apoptosis. In vitro reporter assay suggested EZH2 is a direct target gene of miR-1297. Furthermore, knockdown of EZH2 have the same effect with miR-1297 overeexpression in hepatocellular carcinoma cells. These findings provide evidence that miR-1297 plays a key role in inhibition of the hepatocellular carcinoma cells proliferation, and enhancing cell apoptosis through targeting EZH2, and strongly suggest that ex ogenous miR-1297 may have therapeutic value in treating hepatocellular carcinoma.

Chen P, Wang BL, Pan BS, Guo W
MiR-1297 regulates the growth, migration and invasion of colorectal cancer cells by targeting cyclo-oxygenase-2.
Asian Pac J Cancer Prev. 2014; 15(21):9185-90 [PubMed] Related Publications
Cyclo-oxygenase-2(Cox-2), a key regulator of inflammation-producing prostaglandins, promotes cell proliferation and growth. Therefore, a better understanding of the regulatory mechanisms of Cox-2 could lead to novel targeted cancer therapies. MicroRNAs are strongly implicated in colorectal cancer but their specific roles and functions have yet to be fully elucidated. MiR-1297 plays an important role in lung adenocarcinoma and laryngeal squamous cell carcinoma, but its significance in colorectal cancer (CRC) has yet to be reported. In our present study, we found miR-1297 to be down regulated in both CRC-derived cell lines and clinical CRC samples, when compared with normal tissues. Furthermore, miR-1297 could inhibit human colorectal cancer LOVO and HCT116 cell proliferation, migration, and invasion in vitro and tumorigenesis in vivo by targeting Cox-2. Moreover, miR-1297 directly binds to the 3`-UTR of Cox-2, and the expression level was drastically decreased in LOVO and HCT116 cells following overexpression of miR-1297. Additionally, Cox-2 expression levels are inversely correlated with miR-1297 expression in human colorectal cancer xenograft tissues. These results imply that miR-1297 has the potential to provide a new approach to colorectal cancer therapy by directly inhibiting Cox-2 expression.

Wu XJ, Pu XM, Zhao ZF, et al.
The expression profiles of microRNAs in Kaposi's sarcoma.
Tumour Biol. 2015; 36(1):437-46 [PubMed] Related Publications
Kaposi's sarcoma (KS) is a multicentric angioproliferative tumor of mesenchymal origin. The molecular and biologic aspects of KS are not fully understood. MicroRNAs are non-protein-coding small RNAs in the size range 19-25 nucleotides (nt) that play important roles in biological processes, including cellular differentiation, proliferation, and death. We performed a miRNA microarray analysis by detecting six paired KS and matched adjacent healthy tissues using the 7th generation of miRCURY(TM) LNA Array (v.18.0) (Exiqon) containing 3100 capture probes. We selected 10 significant differentially expressed miRNAs, which were confirmed by quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR) in 18 paired KS and matched adjacent healthy tissue specimens. We also investigated the associations between clinical features and miRNA expression. Among the 3100 human miRNA probes in the microarrays, we identified 170 differentially expressed miRNAs (69 upregulated and 101 downregulated miRNAs) in KS versus adjacent healthy tissues. Among the most significantly upregulated miRNAs were miR-126-3p, miR-199a-3p, miR-16-5p, and the 13 KSHV-related miRNAs. The most significantly downregulated miRNAs included miR-125b-1-3p and miR-1183. Eight upregulated miRNAs, miR-181b-5p, miR-199a-3p, miR-15a-5p, miR-126-3p, miR-1297, kshv-miR-k12-12-3p, kshv-miR-k12-1-5p, and miR-16-5p, and two downregulated miRNAs, miR-125b-1-3p and miR-1183, were confirmed by qRT-PCR in 18 paired KS samples. The qRT-PCR results for 10 miRNAs were consistent with our microarray results. The miR-125b-1-3p and miR-16-5p had statistically significant associations with HHV-8 and HIV infections in KS. The results of miRNA profiling showed that KS appears to have unique expression patterns when compared with paired adjacent healthy tissues, suggesting that deregulation of miRNAs plays an important role in the progression of KS. These differentially expressed miRNAs may provide novel diagnostic and prognostic tools.

Yang NQ, Zhang J, Tang QY, et al.
miRNA-1297 induces cell proliferation by targeting phosphatase and tensin homolog in testicular germ cell tumor cells.
Asian Pac J Cancer Prev. 2014; 15(15):6243-6 [PubMed] Related Publications
To investigate the role of miR-1297 and the tumor suppressor gene PTEN in cell proliferation of testicular germ cell tumors (TGCT). MTT assays were used to test the effect of miR-1297 on proliferation of the NCCIT testicular germ cell tumor cell line. In NCCIT cells, the expression of PTEN was assessed by Western blotting further. In order to confirm target association between miR-1297 and 3'-UTR of PTEN, a luciferase reporter activity assay was employed. Moreover, roles of PTEN in proliferation of NCCIT cells were evaluated by transfection of PTEN siRNA. Proliferation of NCCIT cells was promoted by miR-1297 in a concentration-dependent manner. In addition, miR-1297 could bind to the 3'-UTR of PTEN based on luciferase reporter activity assay, and reduced expression of PTEN at protein level was found. Proliferation of NCCIT cells was significantly enhanced after knockdown of PTEN by siRNA. miR-1297 as a potential oncogene could induce cell proliferation by targeting PTEN in NCCIT cells.

Zhang C, Chi YL, Wang PY, et al.
miR-511 and miR-1297 inhibit human lung adenocarcinoma cell proliferation by targeting oncogene TRIB2.
PLoS One. 2012; 7(10):e46090 [PubMed] Free Access to Full Article Related Publications
microRNAs (miRNAs) are small noncoding RNAs that regulate genes and contribute to many kinds of human diseases, including cancer. Two miRNAs, miR-511 and miR-1297, were investigated for a possible role in adenocarcinoma based on predicted binding sites for the TRIB2 oncogene by microRNA analysis software, and the pcDNA-GFP-TRIB2-3'UTR vector was constructed to investigate the interaction between TRIB2 and miR-511/1297 in the adenocarcinoma cell line A549. Green fluorescent protein (GFP) expression was estimated by fluorescence microscopy and flow cytometry after A549 cells were co-transfected with miR-511 (or miR-1297) and pcDNA-GFP-TRIB2-3'UTR vector. The expression of GFP in the miR-511- and miR-1297-treated cells was significantly downregulated in contrast with the negative-control (NC) miRNA-treated cells. The decreased expression of TRIB2 was further detected after miR-511 (or miR-1297) treatment by western blotting. The MTT test showed inhibition of A549 cell proliferation and Annexin V-FITC/PI dual staining showed increased apoptosis in the miR-511- and miR-1297-treated cells compared to the NC cultures. A transcription factor downstream of TRIB2, the CCAAT/enhancer-binding protein alpha (C/EBPα), was expression at higher levels after miR-511 (or miR-1297) decreasing TRIB2 expression. Our results illustrate that miR-511 and miR-1297 act as tumor suppressor genes, which could suppress A549 cell proliferation in vitro and in vivo by suppressing TRIB2 and further increasing C/EBPα expression.

Li X, Wang HL, Peng X, et al.
miR-1297 mediates PTEN expression and contributes to cell progression in LSCC.
Biochem Biophys Res Commun. 2012; 427(2):254-60 [PubMed] Related Publications
MicroRNAs (miRNAs) are small noncoding RNAs that regulate gene expression after transcription, and are involved in cancer development. Laryngeal squamous cell carcinoma (LSCC) is one of the most common malignant neoplasms with increasing incidence in recent years. In this paper, we report the overexpression of miR-1297 in LSCC and Hep-2 cells. In addition, PTEN was identified to be directly regulated by miR-1297 through western blot and luciferase activity assay. Furthermore, downregulation of miR-1297 in Hep-2 cells was shown to inhibit cancer cell proliferation, migration, and tumor genesis. Our results document a new epigenetic mechanism for PTEN regulation in LSCC, which is crucial for the development of these tumors.

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