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目的探讨二甲双胍(MET)对结肠癌干细胞增殖、凋亡及CD133表达的影响。方法免疫磁珠法从结肠癌细胞株SW480中分选出结肠癌干细胞,流式细胞仪检测其表面标志物CD133。不同浓度MET干预结肠癌干细胞后,CCK-8检测24、48 h细胞增殖;流式细胞术检测细胞凋亡;Western blot检测CD133蛋白表达。结果不同浓度(1、5、10、20 mmol/L)MET干预后,24 h细胞活力[(89.3±16.5)%vs(61.6±16.8)%vs(45.1±14.7)%vs(35.4±13.7)%]与48 h细胞活力[(68.9±25.5)%vs(38.1±17.4)%vs(23.3±6.5)%vs(17.8±6.3)%]比较,差异有统计学意义(P<0.01);与对照组比较,MET(20 mmol/L)干预后的细胞晚期凋亡率(13.5±3.3)%及总凋亡率(23.6±4.9)%差异有统计学意义(P<0.05或P<0.01);MET(10、20 mmol/L)干预后CD133蛋白表达分别为(0.80±0.23)和(0.33±0.19),与对照组比较差异有统计学意义(P<0.05)。结论 MET抑制结肠癌干细胞增殖、促进其凋亡,减少其表面标志物CD133蛋白表达。
Objective To investigate the effects of metformin on proliferation, apoptosis and CD133 expression of colon cancer stem cells. Methods Colon cancer stem cells were sorted out from colon cancer cell line SW480 by immunomagnetic beads method. The surface marker CD133 was detected by flow cytometry. The proliferation of colon cancer stem cells treated with different concentrations of MET was detected by CCK-8 at 24,48 h, the apoptosis was detected by flow cytometry, and the expression of CD133 protein by Western blot. Results After 24h, the cell viability of [(89.3 ± 16.5)% vs (61.6 ± 16.8)% vs (45.1 ± 14.7)% vs (35.4 ± 13.7) %] Was significantly different from that of 48 h ([68.9 ± 25.5]% vs (38.1 ± 17.4)% vs (23.3 ± 6.5)% vs (17.8 ± 6.3)%] Compared with control group, the rate of late apoptosis (13.5 ± 3.3)% and total apoptosis (23.6 ± 4.9)% after MET (20 mmol / L) intervention was statistically significant (P <0.05 or P <0.01) (0.80 ± 0.23) and (0.33 ± 0.19), respectively, after the intervention of MET (10, 20 mmol / L), the difference was statistically significant compared with the control group (P <0.05). Conclusion MET inhibits the proliferation of colon cancer stem cells, promotes its apoptosis and reduces the expression of its surface marker CD133.