Hongyan Ai1, Wei Zhou1, Zeqiang Wang1, Guo Qiong1, Zhouxi Chen1, Shungang Deng2. 1. Department of Breast surgery, Zhuzhou City Central Hospital, Xiangya Medical College, Certral South University, Zhuzhou, China. 2. Department of General surgery, Zhuzhou City Central Hospital, Xiangya Medical College, Certral South University, Zhuzhou, China.
Abstract
PURPOSE: To investigate the effects of microRNAs-107 (miR-107) on autophagy, proliferation, and migration of breast cancer cells and its mechanism by targeting high mobility group protein B1 (HMGB1). METHODS: Real-time polymerase chain reaction assay was used to detect the expression of miR-107 in breast cancer and its cell lines. In MDA-MB-231 and MDA-MB-453 breast cancer cells, the expression of p62, Beclin1 protein, and the changes of cell proliferation and migration after overexpression of m miR-107 were detected by Western blotting, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, and transwell assays. Target Scan online prediction, dual luciferase reporter gene, and Western blot were used to verify the targeting relationship between miR-107 and HMGB1. The effects of silencing HMGB1 expression on p62, Beclin1 protein expression, cell proliferation, and migration ability were detected. The transfected MDA-MB-453 cells were inoculated into the right axilla of the nude mice, the tumor volume and weight were weighed, and the expression of miR-107, HMGB1, p62, and Beclin1 in the tumor were detected. RESULTS: The expression of miR-107 was downregulated in breast cancer tissues and cell lines (P < 0.01). The expression of p62 protein was upregulated (P < 0.01), while Beclin1 protein was downregulated (P < 0.01) and cell proliferation and migration ability were decreased (P < 0.01) after overexpressing miR-107 in MDA-MB-231 and MDA-MB-453 cells. The results of TargetScan online prediction, dual luciferase reporter gene, and Western blot showed that miR-107 could regulate HMGB1 expression. The expression of p62 protein was upregulated (P < 0.01), while Beclin1 protein was downregulated (P < 0.01) and cell proliferation and migration ability were decreased (P < 0.01) after silencing HMGB1 in MDA-MB-231 and MDA-MB-453 cells. The results of xenograft experiments showed that miR-107 could delay tumor growth and inhibit autophagy. CONCLUSION: miR-107 could inhibit cell autophagy, proliferation, and migration of breast cancer cells by targeting HMGB1.
PURPOSE: To investigate the effects of microRNAs-107 (miR-107) on autophagy, proliferation, and migration of breast cancer cells and its mechanism by targeting high mobility group protein B1 (HMGB1). METHODS: Real-time polymerase chain reaction assay was used to detect the expression of miR-107 in breast cancer and its cell lines. In MDA-MB-231 and MDA-MB-453 breast cancer cells, the expression of p62, Beclin1 protein, and the changes of cell proliferation and migration after overexpression of m miR-107 were detected by Western blotting, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, and transwell assays. Target Scan online prediction, dual luciferase reporter gene, and Western blot were used to verify the targeting relationship between miR-107 and HMGB1. The effects of silencing HMGB1 expression on p62, Beclin1 protein expression, cell proliferation, and migration ability were detected. The transfected MDA-MB-453 cells were inoculated into the right axilla of the nude mice, the tumor volume and weight were weighed, and the expression of miR-107, HMGB1, p62, and Beclin1 in the tumor were detected. RESULTS: The expression of miR-107 was downregulated in breast cancer tissues and cell lines (P < 0.01). The expression of p62 protein was upregulated (P < 0.01), while Beclin1 protein was downregulated (P < 0.01) and cell proliferation and migration ability were decreased (P < 0.01) after overexpressing miR-107 in MDA-MB-231 and MDA-MB-453 cells. The results of TargetScan online prediction, dual luciferase reporter gene, and Western blot showed that miR-107 could regulate HMGB1 expression. The expression of p62 protein was upregulated (P < 0.01), while Beclin1 protein was downregulated (P < 0.01) and cell proliferation and migration ability were decreased (P < 0.01) after silencing HMGB1 in MDA-MB-231 and MDA-MB-453 cells. The results of xenograft experiments showed that miR-107 could delay tumor growth and inhibit autophagy. CONCLUSION:miR-107 could inhibit cell autophagy, proliferation, and migration of breast cancer cells by targeting HMGB1.