首页> 中文期刊> 《实用肿瘤学杂志》 >苏林酸在NF-κB对人乳腺癌TNF-α诱导细胞凋亡增敏中的相关作用

苏林酸在NF-κB对人乳腺癌TNF-α诱导细胞凋亡增敏中的相关作用

         

摘要

目的 探讨苏林酸在NF-κB对人乳腺癌TNF-α诱导细胞凋亡增敏中的相关作用.方法 取对数生长期的人乳腺癌细胞系MCF-7,加入苏林酸,使其终浓度分别为0.5 mmol/L和1.0 mmol/L,并设不加苏林酸的对照组进行培养;苏林酸处理48 h后进行MTT、流式细胞实验和Western blot法检测,分析苏林酸对肿瘤细胞生长的作用与相关机制.结果 0.5 mmol/L和1.0 mmol/L苏林酸分别刺激MCF-7细胞48 h后,对应的MCF-7细胞的增殖抑制率为(29.17±1.23)%、(38.15±1.51)%,对照组为(1.15±0.02)%(P<0.05).与对照组相比,0.5 mmol/L和1.0 mmol/L苏林酸作用后均可导致滞留在G0~G1期的MCF-7细胞显著增加(P<0.05);0.5 mmol/L和1.0 mmol/L苏林酸作用后MCF-7细胞的凋亡率明显增加(P<0.05);0.5 mmol/L和1.0 mmol/L苏林酸作用后TNF-α的相对表达量分别为2.09±0.67、1.18±0.09,明显低于对照组的7.42±0.56(P<0.05).结论 苏林酸具有一定抗人乳腺癌细胞生长的作用,能促使细胞周期G0~G1期延长,提高细胞凋亡增敏作用,其作用机制可能与抑制TNF-α活性有关.%Objective The objective of this study was to investigate the role of sulindac in sensitization effects of NF-κB on apoptosis induced by TNF-α in human breast cancer.Methods The human breast cancer MCF-7 cell line was added sulindal in the logarithmic growth phase and the final concentrations of sulindac were 0.5 and 1.0 mmol/L.The cells in control group was cultured without adding succinic acid.After sulindac treatment for 48 h,flow cytometry,MTT and Western blotting were used to analyze the effect and mechanism of cell growth in MCF-7 cells.Results The inhibitory rate of cell proliferation was(29.17±1.23)% and(38.15±1.51)% in MCF-7 cells treated with 0.5 and 1.0 mmol/L of Sulindac for 48 h,respectively,when compared to the control group(1.15 ± 0.02)%(P<0.05).Compared with the control group,0.5 and 1.0 mmol/L of sulindac were significantly increased the G0/G1 phase in MCF-7 cells(P<0.05).The apoptosis rate of sulindac in MCF-7 cells was significantly higher than that in the control group(P<0.05).The expression levels of TNF-α were(2.09±0.67)% and(1.18±0.09)% in the concentrations of 0.5 and 1.0mmol/L sulindac,respectively,in MCF-7 cells when compared to the control group(7.42±0.56)%.Conclusion Sulindac has a certain effect on the growth of human breast cancer cells,which can promote the prolongation of cell cycle at the G0/G1 phase and improve sensitization of apoptosis.This mechanism may be related to the inhibition of TNF-α activity.

著录项

相似文献

  • 中文文献
  • 外文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号