Abstract 【Objective】 To investigate the effect of polydatin on the proliferation and apoptosis of MDA-MB-231 cells in breast cancer. 【Methods】 Breast cancer MDA-MB-231 cells was treated at different concentrations (0, 2, 4, 6, 8, 16 μmol/L) of polydatin; Cell proliferation was detected by MTT method. Breast cancer MDA-MB-231 cells were divided into control group (routine culture) and polydatin group(6 μmol/L polydatin treatment), polydatin +Anti-NC group (transfection inhibitor control, 6 μmol/L polydatin treatment), polydatin+Anti-miR-181a-5 group (transfected with miR-181a-5 inhibitor, 6 μmol/L polydatin treatment). The apoptosis of MDA-MB-231 cells was detected by flow cytometry, and the expression levels of Bax, c-caspase-3 and caspase-3 proteins in MDA-MB-231 cells were detected by Western blot; The expression level of mir-181a-5p in MDA-MB-231 cells was measured by realtime PCR. 【Results】 Compared with the control group, 2, 4, 6, 8, 16 μmol/L,the absorbance value of cells treated with polydatin decreased significantly (all P<0.05).Compared with polydatin+Anti-NC group, the level of miR-181a-5p in polydatin+Anti-miR-181a-5 group decreased, the absorbance value increased, the apoptosis rate decreased, and the levels of Bax, c-caspase-3, caspase-3 protein in breast cancer cells decreased (P<0.05). Compared with the control group, the apoptosis rate of breast cancer cells in the polydatin group increased, the levels of apoptotic proteins Bax, c-caspase-3 and caspase-3 increased, and the expression level of miR-181a-5p increased (P<0.05). 【Conclusion】Polydatin inhibits the proliferation and induces apoptosis of breast cancer MDA-MB-231 cells by up regulating miR-181a-5p.
LI Fu-cheng,CHEN Xin-chu,LI Guan-cheng. Study on the Mechanism of Apoptosis of MDA-MB-231 Cells Induced by Polydatin in Vitro Mediated by miR-181a-5p[J]. JOURNAL OF CLINICAL RESEARCH, 2022, 39(7): 1014-1017.
[1] DENG X,WU H,GAO F,et al. Brachytherapy in the treatment of breast cancer[J].Int J Clin Oncol,2017,22(4):641-650.
[2] HAO J,HUANG K,CHEN C,et al. Polydatin improves glucose and lipid metabolisms in insulin-resistant HepG2 cells through the AMPK pathway[J].Biol Pharm Bull,2018,41(6):891-898.
[3] 潘纪红,王海滨,杜晓飞,等. 虎杖苷通过P13K/AKT/mTOR信号通路诱导人宫颈癌细胞凋亡的初步研究[J].中国中药杂志,2017,42(12):2345-2349.
[4] 何建苗,赵华洲,王婷,等. miR-181a-5p靶向Kras对乳腺癌细胞MDA-MB-231增殖及凋亡的调控作用[J].解放军医学杂志,2018,43(9):735-739.
[5] SUNG J E,KIM J E,LEE H A,et al. Comparison of therapeutic responses to an anticancer drug in three stocks of ICR mice derived from three different sources[J].Lab Anim Res,2017,33(2):187-194.
[6] INCE S,AVDATEK F,DEMIREL H H,et al. Ameliorative effect of polydatin on oxidative stress-mediated testicular damage by chronic arsenic exposure in rats[J].Andrologia,2016,48(5):518-524.
[7] 王亚运,张琪. 虎杖苷的药理作用研究进展[J].医学综述,2017,23(5):989-991.
[8] JIAO Y,WU Y,DU D,et al. Polydatin inhibits cell proliferation,invasion and migration,and induces cell apoptosis in hepatocellular carcinoma[J].Braz J Med Biol Res,2018,51(4):e6867.
[9] ZHANG Y,ZHUANG Z,MENG Q,et al. Polydatin inhibits growth of lung cancer cells by inducing apoptosis and causing cell cycle arrest[J].Oncol Lett,2014,7(1):295-301.
[10] KIM E M,JUNG C H,KIM J,et al. The p53/p21 complex regulates cancer cell invasion and apoptosis by targeting Bcl-2 family proteins[J].Cancer Res,2017,77(11):3092-3100.
[11] MIAO R,XU X,WANG Z,et al. Synergistic effect of nutlin-3 combined with aspirin in hepatocellular carcinoma HepG2 cells through activation of Bcl-2/Bax signaling pathway[J].Mol Med Rep,2018,17(3):3735-3743.
[12] FENG X,YU Y,HE S,et al. Dying glioma cells establish a proangiogenic microenvironment through a caspase 3 dependent mechanism[J].Cancer Lett,2017,385(1):12-20.
[13] MA Z,XIANG Q,WANG D,et al. MiR-181a-5p inhibits cell proliferation and migration by targeting Kras in non-small cell lung cancer A549 cells[J].Acta Biochim Biophys Sin,2015,47(8):630-638.
[14] KORHAN P,ERDAL E,ATABEY N. MiR-181a-5p is downregulated in hepatocellular carcinoma and suppresses motility,invasion and branching-morphogenesis by directly targeting c-met[J].Biochem Biophys Res Commun,2014,450(4):1304-1312.
2022, Vol. 39 
