ArticleMolecular and cellular biochemistry2017
miR-3117 regulates hepatocellular carcinoma cell proliferation by targeting PHLPPL.
Article in Molecular and cellular biochemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 29 citations in OpenAlex.
- Article
- Identification of a five m6A-relevant mRNAs signature and risk score for the prognostication of gastric cancer.Journal of gastrointestinal oncology · 2022Article
- Oncogenic role ofAutophagy · 2021Article
- DLG1-AS1 is activated by MYC and drives the proliferation and migration of hepatocellular carcinoma cells through miR-497-5p/SSRP1 axis.Cancer cell international · 2021Article
- Association between Genetic Polymorphisms of miR-1307, miR- 1269, miR-3117 and Breast Cancer Risk in a Sample of South East Iranian Women.Asian Pacific journal of cancer prevention : APJCP · 2021Article
- miR-762 Promotes Malignant Development of Head and Neck Squamous Cell Carcinoma by Targeting PHLPP2 and FOXO4.OncoTargets and therapy · 2019Article
- eNOS expression and NO release during hypoxia is inhibited by miR-200b in human endothelial cells.Angiogenesis · 2018Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Altered microRNA expression is associated with tumor proliferation, metastasis, and tumorigenesis. In this study, we studied the role of miR-3117 in hepatocellular carcinoma (HCC) cell proliferation and found that miR-3117 was upregulated in HCC tissues and cells. MTT assay, soft agar growth assay, BrdU assay, and cell cycle assay revealed that miR-3117 overexpression promoted HCC HepG2 cell proliferation and that knockdown of miR-3117 suppressed HepG2 proliferation. Mechanism analysis suggested PH domain and leucine-rich repeat protein phosphatase-like (PHLPPL) as the target of miR-3117. Luciferase reporter assay suggested that miR-3117 directly binds to the 3'UTR of PHLPPL. Double knockdown of miR-3117 and PHLPPL copied the phenotypes caused by miR-3117 overexpression, suggesting that miR-3117 contributes to the proliferation of HepG2 by targeting PHLPPL. Our study provided a target for HCC therapy.
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