ArticleOncotarget2015
Upregulated in Hepatitis B virus-associated hepatocellular carcinoma cells, miR-331-3p promotes proliferation of hepatocellular carcinoma cells by targeting ING5.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 58 citations in OpenAlex.
- A comprehensive overview on the crosstalk between microRNAs and viral pathogenesis and infection.Medicinal research reviews · 2025Review
- Hepatitis E virus infection upregulates ING5 expressionActa biochimica et biophysica Sinica · 2024Article
- The Antitumor and Sorafenib-resistant Reversal Effects of Ursolic Acid on Hepatocellular Carcinoma via Targeting ING5.International journal of biological sciences · 2024Article
- Plasma miRNA profile at COVID-19 onset predicts severity status and mortality.Emerging microbes & infections · 2022Article
- Transcriptional Regulation of ING5 and its Suppressive Effects on Gastric Cancer.Frontiers in oncology · 2022Article
- The roles of ING5 in cancer: A tumor suppressor.Frontiers in cell and developmental biology · 2022Review
- Circular RNA circRASSF5 Functions as an Anti-Oncogenic Factor in Hepatocellular Carcinoma by Acting as a Competitive Endogenous RNA Through Sponging miR-331-3p.Journal of hepatocellular carcinoma · 2022Article
- Cell death pathways and viruses: Role of microRNAs.Molecular therapy. Nucleic acids · 2021Review
- Review
- Diagnostic potential of three serum microRNAs as biomarkers for equine sarcoid disease in horses and donkeys.Journal of veterinary internal medicine · 2021Article
- Octreotide acetate combined with somatostatin upregulates miR-1291 and downregulates miR-331-3p in patients with cirrhosis and upper gastrointestinal bleeding.American journal of translational research · 2021Article
- miR-331 inhibits CLDN2 expression and may alleviate the vascular endothelial injury induced by sepsis.Experimental and therapeutic medicine · 2020Article
- Insight in miRNome of Long-Term Non-Progressors and Elite Controllers Exposes Potential RNAi Role in Restraining HIV-1 Infection.Journal of clinical medicine · 2020Article
- Review
- Potential targets and molecular mechanism of miR-331-3p in hepatocellular carcinoma identified by weighted gene coexpression network analysis.Bioscience reports · 2020Article
- miR-331-3p Inhibits Tumor Cell Proliferation, Metastasis, Invasion by Targeting MLLT10 in Non-Small Cell Lung Cancer.Cancer management and research · 2020Article
- Review
- MicroRNA-331-3p inhibits proliferation and metastasis of ovarian cancer by targeting RCC2.Archives of medical science : AMS · 2019Article
- MicroRNA-331 inhibits development of gastric cancer through targeting musashi1.World journal of gastrointestinal oncology · 2019Article
- microRNAs: Key players in virus-associated hepatocellular carcinoma.Journal of cellular physiology · 2019Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
unlabelledHepatitis B virus (HBV) is a major risk factor for development and progression of hepatocellular carcinoma (HCC). It has been reported that viral infection can interfere with cellular microRNA (miRNA) expression and participate in the pathogenesis of oncogenicity. Our miRNAs array data indicated that miR-331-3p expression in HCC cell lines increased, but the relationship between miR-331-3p expression and HBV activity is unclear. Here, we observed elevated expression of miR-331-3p in different HCC cell lines expressing HBV. HBV, especially HBx, promotes miR-331-3p expression by enhancing its promoter activity. Using a miRNA target prediction database miRBase, we identified ING5 to be a novel target gene of miR-331-3p. miR-331-3p could inhibit ING5 expression by directly targeting its 3'-untranslated region (3'-UTR). As predicted, HBV was confirmed to repress ING5 at both mRNA and protein levels by promoting miR-331-3p expression. Our result indicated that miR-331-3p expression promotes proliferation of SMMC7721 cells by inhibiting ING5. ING5 overexpression promoted cell apoptosis in HCC cell lines. We also found ING5 expression was decreased in tumor tissue of HCC patient with HBV infection compared to its expression in para-carcinoma tissues.
conclusionThese results showed that miR-331-3p is upregulated by HBV and promotes proliferation of HCC cells though repression of ING5 expression. These data provide new insights for understanding the mechanisms of HBV-related HCC pathogenesis.
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Registered trials
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