Open Access

ARTICLE

MicroRNA-142-5p Overexpression Inhibits Cell Growth and Induces Apoptosis by Regulating FOXO in Hepatocellular Carcinoma Cells

Kexin Lou^*1, Ning Chen^†1, Zhihong Li^*, Bei Zhang^†, Xiuli Wang^‡, Ye Chen^*, Haining Xu^*, Dongwei Wang^*, Hao Wang^*

* Department of Ultrasound, Xuzhou Central Hospital, Xuzhou, Jiangsu, P.R. China
† Department of Gynecology and Obstetrics, Xuzhou Central Hospital, Xuzhou, Jiangsu, P.R. China
‡ Central Laboratory, Xuzhou Central Hospital, Xuzhou, Jiangsu, P.R. China
1 These authors provided equal contribution to this work

Oncology Research 2017, 25(1), 65-73. https://doi.org/10.3727/096504016X14719078133366

Retracted 25 July 2024

Abstract

Abnormal expression of microRNA (miR)-142-5p has been reported in hepatocellular carcinoma (HCC). However, little information is available regarding the functional role of miR-142-5p in HCC. We aimed to explore the effects of miR-142-5p aberrant expression on HCC cell growth and cell apoptosis, as well as the underlying mechanism. Human HCC cell lines HepG2 and SMMC-7721 cells were transfected with miR- 142-5p mimic, inhibitor, or a corresponding negative control. Cell viability, cell cycle distribution, and cell apoptosis were then analyzed. In addition, protein expression of Forkhead box, class O (FOXO) 1 and 3, a Bcl-2-interacting mediator of cell death (Bim), procaspase 3, and activated caspase 3 was measured. After transfection with miR-142-5p inhibitor, FOXO1 and FOXO3 were overexpressed, and then the cell viability and cell apoptosis were determined again. The relative cell viability in both HepG2 and SMMC-7721 cells was significantly reduced by miR-142-5p overexpression (p < 0.05). miR-142-5p overexpression displayed a significant blockage at the G₁/S transition and significantly increased the percentages of G₀/G₁ phase. Moreover, the results showed that miR-142-5p overexpression significantly induced cell apoptosis and statistically elevated the protein expression levels of FOXO1, FOXO3, Bim, procaspase 3, and activated caspase 3. However, the cells transfected with miR-142-5p inhibitor showed contrary results. Additionally, the effects of miR-142-5p inhibitor on cell viability and apoptosis were reversed by overexpression of FOXO. In conclusion, our results suggest that miR-142-5p overexpression shows an important protective role in HCC by inhibiting cell growth and inducing apoptosis. These effects might be by regulating FOXO expression in HCC cells.

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