Open Access

ARTICLE

Function of miR-152 as a Tumor Suppressor in Human Breast Cancer by Targeting PIK3CA

by

* Second Department of Breast and Thyroid Surgery, Dalian Municipal Central Hospital Affiliated to Dalian Medical University, Dalian, P.R. China
† Department of General Surgery, The Third People’s Hospital of Dalian, Dalian, P.R. China
‡ Department of Thoracic Surgery, Dalian Municipal Central Hospital Affiliated to Dalian Medical University, Dalian, P.R. China

Oncology Research 2017, 25(8), 1363-1371. https://doi.org/10.3727/096504017X14878536973557

Retracted 05 September 2024

Abstract

miR-152, as a tumor suppressor, has been reported to be downregulated in a number of cancer cell lines and tumor tissues, including breast cancer. This study aimed to investigate the role of miR-152 in human breast cancer and its underlying mechanisms. Human breast cancer cell line HCC1806 was transfected with hsa-miR- 152-3p mimic, inhibitor, or scrambled negative controls. The efficiency of miR-152-3p transfection was evaluated by quantitative real-time PCR, and the effects on cell viability and apoptosis as well as on the PI3K/AKT signaling pathway were investigated by MTT assay, flow cytometry, and Western blot analysis, respectively. The binding effect of miR-152-3p on PIK3CA 3'-UTR was also investigated. The results suggested that miR- 152-3p mimic transfection inhibited cell viability while inducing apoptosis of HCC1806 cells. Furthermore, miR-152-3p negatively regulated PIK3CA expression via binding to the 3'-UTR of PIK3CA and decreased the phosphorylation levels of AKT (Ser473) and RPS6 (Ser235/236) in HCC1806 cells. miR-152-3p inhibitor transfection showed the opposite effects. In conclusion, miR-152-3p might serve as a tumor suppressor in human breast cancer cells via negatively regulating PIK3CA expression to inhibit the activation of AKT and RPS6, leading to suppression of HCC1806 cell proliferation.

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Keywords

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