OBJECTIVE: This study aimed at investigating whether miR-637 could promote proliferation of hepatocarcinoma cells by targeted regulation of AKT1 expression, leading to enhanced cell invasion and thus participating in the progression of liver cancer.
PATIENTS AND METHODS: The miR-637 and AKT1 expressions in cancer tissues and adjacent tissues of liver cancer patients were detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The effects of miR-637 on cell proliferation and cell invasion were examined by cell counting kit-8 (CCK-8) and cell invasion assays. Dual-luciferase reporter gene assay was performed to evaluate the regulating relationship between miR-637 and AKT1. Also, the expression of AKT1 after overexpression or knockdown of miR-637 was analyzed by Western blot to evaluate whether miR-637 could affect proliferative and invasive ability of hepatoma cells by inhibiting the expression of AKT1.
RESULTS: The qRT-PCR results revealed that miR-637 expression in cancer tissues of liver cancer patients was markedly lower than that in corresponding adjacent tissues, which was consistent with its low expression in HCC cell lines. However, AKT1 expression in cancer tissues was markedly higher than that in corresponding adjacent tissues. Overexpression of miR-637 in hepatoma cells inhibited cell proliferation and attenuated cell invasion, while inhibition of miR-637 showed the opposite effect. Results of dual-luciferase reporting assay and Western blot demonstrated that miR-637 can selectively degrade AKT1 and that overexpression of AKT1 in HCC cells can partially reverse the effect of miR-637 on cell proliferation and invasion.
CONCLUSIONS: MiR-637 can promote the proliferation of hepatoma cells and enhance invasive cell ability, the mechanism of which may be related to the targeted regulation of AKT1 expression.Free PDF Download
To cite this article
Y.-M. Du, Y.-B. Wang
MiR-637 inhibits proliferation and invasion of hepatoma cells by targeted degradation of AKT1
Eur Rev Med Pharmacol Sci
Vol. 23 - N. 2