Research IndicatorsGraph generated 11 March 2017 using data from PubMed using criteria.
Mouse over the terms for more detail; many indicate links which you can click for dedicated pages about the topic. Tag cloud generated 11 March, 2017 using data from PubMed, MeSH and CancerIndex
Specific Cancers (8)
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).
Numbers shown below represent number of publications held in OncomiRDB database for Oncogenic and Tumor-Suppressive MicroRNAs.
|Tissue||Target Gene(s)||Regulator(s)||MIR1297 Function in Cancer||Effect|
-lung cancer (1)
|TRIB2 (1)||inhibit cell proliferation (1)||tumor-suppressive
|head and neck (1)|
-laryngeal squamous cell carcinoma (1)
|PTEN (1)||promote cell proliferation (1)|
promote cell migration (1)
promote tumorgenesis (1)
Source: OncomiRDB Wang D. et al. Bioinformatics 2014, 30(15):2237-2238.
miRBase, University of Manchester
Annotated database entry including the location and sequence of the mature miRNA sequence.
miRCancer, East Carolina University
Search miRCancer for miR-1297 associations with cancer and associated genes.
International Cancer Genome Consortium.
Summary of gene and mutations by cancer type from ICGC
COSMIC, Sanger Institute
Somatic mutation information and related details
GEO Profiles, NCBI
Search the gene expression profiles from curated DataSets in the Gene Expression Omnibus (GEO) repository.
Latest Publications: MIR1297 (cancer-related)
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
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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 XMiR-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
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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.
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 WMiR-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
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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
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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.
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
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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.