@Article{096504017X14878536973557,
AUTHOR = {Shuke Ge, Dan Wang, Qinglong Kong, Wei Gao, Jiayi Sun},
TITLE = {Function of miR-152 as a Tumor Suppressor in Human Breast Cancer  by Targeting PIK3CA},
JOURNAL = {Oncology Research},
VOLUME = {25},
YEAR = {2017},
NUMBER = {8},
PAGES = {1363--1371},
URL = {http://www.techscience.com/or/v25n8/56921},
ISSN = {1555-3906},
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.},
DOI = {10.3727/096504017X14878536973557}
}