Gao, Dongkai and Zhou, Zumo and Huang, Heqing (2019) miR-30b-3p Inhibits Proliferation and Invasion of Hepatocellular Carcinoma Cells via Suppressing PI3K/Akt Pathway. Frontiers in Genetics, 10. ISSN 1664-8021
pubmed-zip/versions/2/package-entries/fgene-10-01274-r1/fgene-10-01274.pdf - Published Version
Download (3MB)
Abstract
Background: The micro-RNA miR-30b-3p has been reported to play a crucial role in several cancers. However, the biological function of miR-30b-3p in hepatocellular carcinoma (HCC) is still unknown.
Methods: RT-qPCR was employed to determine the expression of miR-30b-3p in HCC tissues and cells. The MTT assay, colony formation assay, and cell migration and invasion assay were employed to evaluate the role of miR-30b-3p in HCC cells. A dual-luciferase reporter assay was employed to verify the target of miR-30b-3p. Western blotting was employed to determine the expression of key molecular signal transducers along TRIM27-PI3K/Akt axis.
Results: Expression of miR-30b-3p was markedly decreased in HCC tissues and cells and positively correlated with higher overall survival. Moreover, miR-30b-3p overexpression significantly repressed cell viability, proliferation, migration, and invasion of HCC cells in vitro. Notably, we demonstrated that miR-30b-3p directly bound to the 3′-untranslated region of tripartite motif containing 27 (TRIM27) mRNA by downregulating the expression of TRIM27, which was demonstrated to be negatively correlated with miR-30b-3p expression. TRIM27 was demonstrated to have an oncogenic role in HCC cells by enhancing cell viability, proliferation, migration, and invasion. Finally, the miR-30-3p-TRIM27-PI3K/Akt axis was shown to play a crucial role in HCC cells in vitro.
Conclusion: Our results indicated that miR-30-3p might act as a new biomarker for the future diagnosis and treatment HCC.
Item Type: | Article |
---|---|
Subjects: | South Archive > Medical Science |
Depositing User: | Unnamed user with email support@southarchive.com |
Date Deposited: | 21 Feb 2023 09:53 |
Last Modified: | 31 Jul 2024 13:40 |
URI: | http://ebooks.eprintrepositoryarticle.com/id/eprint/163 |