ArticleOncotarget2016
miR-214/199a/199a* cluster levels predict poor survival in hepatocellular carcinoma through interference with cell-cycle regulators.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 27 citations in OpenAlex.
- Retraction Note: Forkhead box (FOX) G1 promotes hepatocellular carcinoma epithelial-Mesenchymal transition by activating Wnt signal through forming T-cell factor-4/Beta-catenin/FOXG1 complex.Journal of experimental & clinical cancer research : CR · 2023Article
- A review on the role of cyclin dependent kinases in cancers.Cancer cell international · 2022Review
- MicroRNA-214 enriched exosomes from human cerebral endothelial cells (hCEC) sensitize hepatocellular carcinoma to anti-cancer drugs.Oncotarget · 2021Article
- The Effect of miR-98 and miR-214 on Apoptotic and Angiogenic Pathways in Hepatocellular Carcinoma HepG2 Cells.Indian journal of clinical biochemistry : IJCB · 2020Article
- Interstitial microRNA miR-214 attenuates inflammation and polycystic kidney disease progression.JCI insight · 2020Article
- Construction of microRNA-messenger networks for human osteosarcoma.Journal of cellular physiology · 2019Article
- Integrated analysis of lncRNA-associated ceRNA network reveals potential biomarkers for the prognosis of hepatitis B virus-related hepatocellular carcinoma.Cancer management and research · 2019Article
- miR-214 regulates papillary thyroid carcinoma cell proliferation and metastasis by targeting PSMD10.International journal of molecular medicine · 2018Article
- Expression of the Long Intergenic Non-Protein Coding RNA 665 (LINC00665) Gene and the Cell Cycle in Hepatocellular Carcinoma Using The Cancer Genome Atlas, the Gene Expression Omnibus, and Quantitative Real-Time Polymerase Chain Reaction.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- Inhibition of ATG12-mediated autophagy by miR-214 enhances radiosensitivity in colorectal cancer.Oncogenesis · 2018Article
- PPARBioMed research international · 2018Article
- Cluster of specified microRNAs in tissues and serum as biomarkers for early diagnosis of hepatocellular carcinoma.International journal of clinical and experimental pathology · 2018Article
- Article
- Thyroid hormone inhibits growth of hepatoma cells through induction of miR-214.Scientific reports · 2017Article
- GTSE1 promotes cell migration and invasion by regulating EMT in hepatocellular carcinoma and is associated with poor prognosis.Scientific reports · 2017Article
- New Insights into the Epigenetics of Hepatocellular Carcinoma.BioMed research international · 2017Review
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsTo identify the clinical and functional association of miR-214/199a/199a* cluster in human hepatocellular carcinoma (HCC) and to clarify the mechanism of miR-214.
methodsKaplan-Meier and Cox proportional regression analyses were used to determine the association of miR-214/199a/199a* cluster levels with the survival of HCC patients. The role of miR-214 in regulating HCC cell proliferation was studied with miR-214 mimics/inhibitor-treated cells. Furthermore, the inhibition effect of miR-214 on E2F2, cyclin-dependent kinase (CDK) 3 and CDK6 expression was assessed in HCC cell lines with miR-214 mimics/inhibitors to increase/decrease miR-214 expression. Direct binding of miR-214 to the 3'-untranslated regions of E2F2, CDK3, and CDK6 was verified by dual-luciferase reporter assay.
resultsIn analyzing HCC clinical specimens and cell lines, we discovered a uniform decrease in miR-214/199a/199a* expression in comparison with noncancerous tissue or normal liver epithelial cell lines. Higher miR-214 levels were related with improved patient survival. Overexpression of miR-214 in HCC cells inhibited proliferation by inducing G1-S checkpoint arrest. Conversely, RNA interference-mediated silencing of miR-214 promoted cell-cycle progression and accelerated the proliferation of HCC cells. E2F2, CDK3 and CDK6 were each directly targeted for inhibition by miR-214, and restoring their expression reversed miR-214 inhibition of cell-cycle progression. The relationship between expression of miR-214 and its targets was confirmed in HCC tumor xenografts and clinical specimens.
conclusionsOur results demonstrate that miR-214 has tumor-suppressive activity in HCC through inhibition of E2F2, CDK3 and CDK6.
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