miR-181a-5p介导虎杖苷体外诱导乳腺癌MDA-MB-231细胞凋亡的机制研究

doi:10.3969/j.issn.1671-7171.2022.07.015

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摘要【目的】探讨虎杖苷体外干预对乳腺癌MDA-MB-231细胞增殖及凋亡的影响。【方法】以不同浓度(0、2、4、6、8、16 μmol/L)的虎杖苷处理乳腺癌MDA-MB-231细胞,MTT方法检测细胞增殖变化。乳腺癌MDA-MB-231细胞分成对照组(常规培养)、虎杖苷组(6 μmol/L虎杖苷处理)、虎杖苷+Anti-NC组(转染inhibitor control,6 μmol/L虎杖苷处理)、虎杖苷+Anti-miR-181a-5组(转染miR-181a-5 inhibitor,6 μmol/L虎杖苷处理)。流式细胞术检测MDA-MB-231细胞凋亡情况,Western blot检测MDA-MB-231细胞Bax和c-caspase-3、caspase-3蛋白表达水平,Realtime PCR方法测定MDA-MB-231细胞miR-181a-5p 表达水平。【结果】与对照组比较,2、4、6、8、16 μmol/L的虎杖苷处理后的细胞吸光值显著降低(均P<0.05)。与虎杖苷+Anti-NC组比较,虎杖苷+Anti-miR-181a-5组乳腺癌细胞中miR-181a-5p 水平降低,吸光值升高,细胞凋亡率降低,细胞中Bax、c-caspase-3、caspase-3蛋白水平降低(P<0.05)。与对照组比较,虎杖苷组乳腺癌细胞凋亡率升高,细胞中凋亡蛋白Bax、c-caspase-3、caspase-3水平升高,miR-181a-5p 表达水平升高(P<0.05)。【结论】虎杖苷通过上调miR-181a-5p 抑制乳腺癌MDA-MB-231细胞增殖并诱导细胞凋亡。

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	李釜丞
	陈杏初
	李官成

关键词 ：乳腺肿瘤/病理学, 微RNAs, 虎杖, 细胞凋亡

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.

Key words： Breast Neoplasms/PA MicroRNAs POLYGONUM CUSPIDATUM Apoptosis

收稿日期: 2022-05-12

中图分类号:

R737.9

引用本文:

李釜丞, 陈杏初, 李官成. miR-181a-5p介导虎杖苷体外诱导乳腺癌MDA-MB-231细胞凋亡的机制研究[J]. 医学临床研究, 2022, 39(7): 1014-1017.
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. JOURNAL OF CLINICAL RESEARCH, 2022, 39(7): 1014-1017.

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http://journal07.magtech.org.cn/yxlcyj/CN/10.3969/j.issn.1671-7171.2022.07.015 或 http://journal07.magtech.org.cn/yxlcyj/CN/Y2022/V39/I7/1014

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