Overexpression of miR-3196 suppresses cell proliferation and induces cell apoptosis through targeting ERBB3 in breast cancer
Z.-C. Ji, S.-H. Han, Y.-F. Xing Department of General Surgery, Changji Huizu People’s Hospital of Xinjiang, Xinjiang, China. 15829890388@139.com
OBJECTIVE: Breast cancer is one of the most common malignancies worldwide. MicroRNAs (MiRNAs) have been identified to influence cell behaviors through epigenetic post-transcriptional gene regulation. Therefore, the aim of this study was to determine the role of miR-3196 in the proliferation and apoptosis of breast cancer.
MATERIALS AND METHODS: Human breast cancer cell lines (MCF-7 and MDA-MB-231) were obtained and cultured. The expression level of miR-3196 in breast cancer tissues was detected using Real Time-Polymerase Chain Reaction (RT-PCR). The effects of miR-3196 on the proliferation and apoptosis of breast cancer cells were analyzed by cell counting kit-8 (CCK-8) assay and TUNEL assay, respectively. In addition, the interaction between miR-3196 expression and erb-b2 receptor tyrosine kinase 3 (ERBB3) expression, as well as the mechanism of miR-3196 regulating ERBB3 in breast cancer, were also addressed by RT-PCR, Western blot, and luciferase reporter gene assay.
RESULTS: MiR-3196 was lowly expressed in breast cancer tissues. Overexpression of miR-3196 could repress the proliferation and induce the apoptosis of breast cancer cells via targeting the 3’UTR of ERBB3.
CONCLUSIONS: Our findings provide novel insights into the role of miR-3196 in breast cell proliferation and apoptosis. Meanwhile, this study suggests that miR-3196 can serve as a potential biomarker and therapeutic target for breast cancer.
Free PDF DownloadThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License
To cite this article
Z.-C. Ji, S.-H. Han, Y.-F. Xing
Overexpression of miR-3196 suppresses cell proliferation and induces cell apoptosis through targeting ERBB3 in breast cancer
Eur Rev Med Pharmacol Sci
Year: 2018
Vol. 22 - N. 23
Pages: 8383-8390
DOI: 10.26355/eurrev_201812_16536