Scimago Lab
powered by Scopus
call: +1.631.470.9640
Mon-Fri 10 am - 2 pm EST


Medical Science Monitor Basic Research


eISSN: 1643-3750

Get your full text copy in PDF

mir-129-5p Attenuates Irradiation-Induced Autophagy and Decreases Radioresistance of Breast Cancer Cells by Targeting HMGB1

Jing Luo, Jie Chen, Li He

(Department of Breast Surgery, Sichuan Academy of Medical Science & Sichuan Provincial People’s Hospital, School of Clinical Medicine, University of Electronic Science and Technology of China, Chengdu, Sichuan, China (mainland))

Med Sci Monit 2015; 21:4122-4129

DOI: 10.12659/MSM.896661

BACKGROUND: This study aimed to determine the role of miR-129-5p in irradiation-induced autophagy in breast cancer cells and to investigate its downstream regulation in autophagy-related radiosensitivity.
MATERIAL AND METHODS: Relative miR-129-5p expression in breast cancer cell lines MCF-7, MDA-MB-231, BT474, and BT549, and in 1 non-tumorigenic breast epithelial cell line, MCF-10A, was compared. The effect of miR-129-5p on irradiation-induced autophagy and radiosensitivity of the cancer cells was explored. The regulative effect of miR-129-5p on HMGB1 and the functional role of this axis in autophagy and radiosensitivity were also studied.
RESULTS: Ectopic expression of miR-129-5p sensitized MDA-MD-231 cells to irradiation, while knockdown of miR-129-5p reduced radiosensitivity of MCF-7 cells. MiR-129-5p overexpression inhibited irradiation-induced autophagy. HMGB1 is a direct functional target of miR-129-5p in breast cancer cells. MiR-129-5p may suppress autophagy and decrease radioresistance of breast cancer cells by targeting HMGB1.
CONCLUSIONS: The miR-129-5p/HMGB1 axis can regulate irradiation-induced autophagy in breast cancer and might be an important pathway in regulating radiosensitivity of breast cancer cells.

This paper has been published under Creative Common Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) allowing to download articles and share them with others as long as they credit the authors and the publisher, but without permission to change them in any way or use them commercially.
I agree