title: mir-129-5p Attenuates Irradiation-Induced Autophagy and Decreases Radioresistance of Breast Cancer Cells by Targeting HMGB1.
abstract: 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.
authors.affiliation: 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).
authors.forename: Jing
authors.initials: J
authors.lastname: Luo
authors.affiliation: Graduate School, Zunyi Medical University, Zunyi, Guizhou, China (mainland).
authors.forename: Jie
authors.initials: J
authors.lastname: Chen
authors.affiliation: Department of Breast Surgery, Sichuan Academy of Medical Science & Sichuan Provincial People's Hospital (East), School of Clinical Medicine, University of Electronic Science and Technology of China, Chengdu, Sichuan, China (mainland).
authors.forename: Li
authors.initials: L
authors.lastname: He
mesh_terms: D017209:Apoptosis / Q000235:genetics / Q000528:radiation effects; D001343:Autophagy / Q000235:genetics / Q000528:radiation effects; D001943:Breast Neoplasms / Q000235:genetics / Q000378:metabolism* / Q000473:pathology / Q000532:radiotherapy*; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000235:genetics / Q000528:radiation effects; D005260:Female; D024243:HMGB1 Protein / Q000235:genetics / Q000378:metabolism*; D006801:Humans; D061986:MCF-7 Cells; D035683:MicroRNAs / Q000235:genetics / Q000378:metabolism*; D011836:Radiation Tolerance
chemical_list: D024243:HMGB1 Protein; C585491:HMGB1 protein, human; D035683:MicroRNAs; C541915:Mirn129 microRNA, human