羟基喜树碱依赖Caspase3途径诱导人乳腺癌Bcap37细胞凋亡

Role of Caspase3 in apoptosis induced by HCPT in human breast carcinoma cells

目的:探讨羟基喜树碱(HCPT)诱导人乳腺癌Bcap37细胞凋亡所涉及的信号转导途径.方法:采用MTT法测定细胞的增殖活力,琼脂糖凝胶电泳观察细胞调亡,流式细胞仪进行细胞周期分析,Western blot法研究细胞调亡途径.结果:HCPT对Bcap-37有明显的生长抑制作用.10～100 μmol·L-1HCPT作用细胞后,琼脂糖凝胶电泳检测到典型的DNA梯状条带.Caspase3在细胞凋亡过程中发生降解,Caspase3抑制剂DEVD-CHO可抑制HCPT诱导的Caspase3的降解和细胞凋亡.结论:HCPT对Bcap-37有明显的生长抑制和诱导调亡作用.Caspase3在HCPT诱导人乳腺癌Bcap37细胞调亡中起着重要作用.

AIM： To investigate the role of Caspase3 in apoptosis induced by HCPT in human breast carcinoma cells. METHODS： The cell growth inhibiting was measured by MTT assay, cell apoptosis was investigated by agarose gel eletrophoresis, and apoptosis pathway was investigated by Western Blotting. RESULTS： HCPT had a remarkable growth inhibiting on breast cancer cells. After exposing to HCPT, the breast cancer cells present some morphologic features of apoptosis that including cell shrinkage, nuclear condensation, DNA fragmentation. Caspase3 was degraded in cancer cells treated with HCPT. CONCLUSION： HCPT has obvious effects on growth inhibiting and apoptosis induction on human breast cancer cells, and the altered expression of Caspase3 may play a significant role in apoptosis induced by HCPT.