ArticleOncoTargets and therapy2019
MicroRNA-3651 promotes the growth and invasion of hepatocellular carcinoma cells by targeting PTEN.
Article in OncoTargets and therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 5 citations in OpenAlex.
- Clinical significance of circulatory microRNA-183_5p and 3651 in serum as novel potential diagnostic marker for gallbladder cancer.Indian journal of gastroenterology : official journal of the Indian Society of Gastroenterology · 2026Article
- Non-viral HCC miRNA profiling reveals miR-1972 as a potential positive prognostic marker.Non-coding RNA research · 2025Article
- Article
- Hsa-miR-3651 could serve as a novel predictor for in-breast recurrence via FRMD3.Breast cancer (Tokyo, Japan) · 2022Article
- miR-3651 Participates in the Growth Cycle of Hepatocellular Carcinoma Cells and Promotes the Malignant Metastasis via the PI3K/AKT/mTOR Signalling Pathway.Journal of oncology · 2022Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHepatocellular carcinoma (HCC) is one of the most common malignant tumors in human worldwide. Evidence indicated that upregulation of microRNA-3651 (miR-3651) was observed in human HCC tissues. In this study, we explored the mechanisms by which miR-3651 regulated the proliferation, apoptosis and invasion of HCC.
methodsThe levels of miR-3651 in human HCC tissues were detected using qRT-PCR assay. In addition, transwell invasion and Western blot assay were conducted to detect cell invasion and apoptosis, respectively. Meanwhile, the dual-luciferase reporter assay was used to explore the interaction of miR-3651 and phosphate and tension homology deleted on chromsome ten (PTEN) in HCC.
resultsThe levels of miR-3651 were upregulated in HCC tissues in comparison with the matched normal tissues. Overexpression of miR-3651 significantly promoted the proliferation and invasion of Huh-7 cells. In contrast, inhibition of miR-3651 markedly inhibited the proliferation and invasion of Huh-7 cells via promoting apoptosis. Moreover, downregulation of miR-3651 markedly inhibited tumor growth in vivo. Furthermore, bioinformatics analysis and luciferase reporter assay identified that PTEN was the directly binding target of miR-3651 in Huh-7 cells. Meanwhile, overexpression of miR-3651 obviously decreased the level of PTEN, and increased the expressions of p-p85 and p-Akt in Huh-7 cells.
conclusionThese results indicated that miR-3651 might act as a potential oncogene in HCC by targeting PTEN. Therefore, miR-3651 might be a novel therapeutic target for the treatment of HCC.
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