临床肿瘤学杂志

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西达本胺对三阴性乳腺癌细胞凋亡和侵袭的影响

施秀青1,马飞2,李慧慧1,王海娟3,张雪燕3,林晨3,钱海利2,徐兵河2   

  1. 1 北京协和医学院中国医学科学院肿瘤医院内科 2 中国医学科学院肿瘤医院肿瘤研究所 3 中国医学科学院肿瘤研究所分子肿瘤学国家重点实验室
  • 收稿日期:2013-07-01 修回日期:2013-09-09 出版日期:2013-12-31 发布日期:2013-12-31
  • 通讯作者: 徐兵河

Effect of chidamide on apoptosis and infiltration in triple negative breast cancer cell

SHI Xiuqing, MA Fei, LI Huihui, WANG Haijuan, ZHANG Xueyan, LIN Chen, QIAN Haili, XU Binghe   

  • Received:2013-07-01 Revised:2013-09-09 Online:2013-12-31 Published:2013-12-31
  • Contact: XU Binghe

摘要: 目的 探讨组蛋白去乙酰化酶抑制剂(HDACi)西达本胺对三阴性乳腺癌细胞株CAL51体外增殖、凋亡及侵袭的作用。方法 采用实时无标记细胞分析(RTCA)技术检测不同浓度西达本胺(0、5、10、20、50、100μmol/L)对CAL51细胞的增殖抑制作用;倒置显微镜下观察西达本胺(10、15、20μmol/L)处理CAL51细胞72h后的细胞形态;流式细胞仪检测细胞周期、凋亡及乳腺癌干细胞比例;采用RTCA技术检测西达本胺对细胞侵袭、浸润能力的影响。结果 西达本胺在体外能明显抑制CAL51细胞的增殖,且与药物浓度呈正相关(r=0.791,P<0.001);细胞形态发生改变;流式细胞仪检测显示细胞出现明显凋亡,且随药物浓度、作用时间的增加而升高(P<0.05),细胞周期和干细胞比例无变化;西达本胺对CAL-51细胞的侵袭、浸润能力有抑制作用,且随着药物浓度的增加,细胞侵袭能力明显降低(P<0.05)。结论 西达本胺能够明显抑制CAL-51细胞的生长,诱导其凋亡,并降低其侵袭、浸润能力。

Abstract: Objective To investigate the effects of histone deacetylase inhibitor(HDACi), chidamide, on proliferation, apoptosis and infiltration in triple negative breast cancer CAL51 cell line in vitro. Methods The real time cellular analysis (RTCA) assay was employed to detect proliferation inhibition efficiency by treating cells with different concentration groups of chidamide (0, 5, 10, 20, 50, 100μmol/L). When CAL-51 cells were treated with chidamide (10, 15, 20μmol/L) for 72h, morphological changes of CAL-51 were observed under inverse microscopy. The cell apoptosis, cell cycles and stem cell proportion were analyzed by flow cytometry. RTCA assay was used to detect changes of infiltration ability after treatment. Results Chidamide was able to inhibit proliferation of CAL51 cells in vitro in a positive concentration dependent manner (r=0.791,P<0.001). After being treated with chidamide, cell morphology appeared great changes. Flow cytometry assay showed obvious apoptosis compared with control group with the increase of drug concentration and acting hours (P<0.05), but no alternation of cell cycles and stem cell proportion were detected. RTCA assay showed that cell infiltration ability was obviously inhibited after treatment. With the increase of drug concentration, the inhibition of cell invasion ability increased significantly (P<0.05). Conclusion Chidamide can obviously inhibit the proliferation of CAL-51 cells, induce its apoptosis and reduce the cell invasion and infiltration capacity.

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