【摘要】 目的　探讨阿霉素(ADM)对人乳腺癌细胞株Bcap37、MDA- MB -231的抑制作用效果及机制,评估细胞凋亡对乳腺癌治疗应用价值。方法　应用不同浓度阿霉素作用于Bcap37、MDA- MB -231,用MTT法检测抑制率,流式细胞术(FCM)检测细胞凋亡及凋亡相关分子Fas、Bcl- 2与突变型p53蛋白表达的变化。结果　阿霉素对Bcap37的抑制率较高并呈剂量和时间依赖性,但对MDA -MB -231抑制率较低,且剂量和时间效应关系不明显。阿霉素作用于Bcap37后Fas表达升高,Bcl- 2表达降低,可观察到细胞凋亡。阿霉素作用于MDA- MB -231后p53、Fas、Bcl -2表达变化不明显,未发现凋亡细胞。结论　不同的乳腺癌细胞株由于其分子生物学特性不同,对化疗敏感性、抗药性不同,与化疗药物对其诱导凋亡的能力差异有关,为乳腺癌的个体化治疗提供实验依据。更多还原

【Abstract】 Objective To investigate the inhibitory and apoptosis regulating effects of adr iamycin (ADM) on different human breast cancer cell lines and to evaluate the va lue of apoptosis in breast cancer treatment. Methods Human breast cancer cells of the lines Bcap37 and MDA-MB-231 were c ultured. ADM of different concentrations was added into the culture fluid. MTT m ethod was used to detect the inhibition rate. Flow cytometry was used to detect the proliferation and apoptosis of the cells. To examine the expression of apopt osis-related molecules: Fas, mutant p53, and Bcl-2 proteins. Results ADM inhibited the proliferation of Bcap37 cells and MDA-MB-231 cell s dose and time-dependently, however, the inhibitory effect of ADM was stronger on the Bcap37 cells than on the MDA-MB-231 cells. After being treated by ADM the expression of Fas was increased and the expression of Bcl-2 was decreased i n the Bcap37 cells. However, after being treated by ADM the expressions of Fas, Bcl-2, and mutant p53 in the MDA-MB-231 cells remained almost unchanged. Trea ted by ADM for 24 hours the apoptotic rate of the Bcap37 cells was increased fro m 0% to 5.8% (P<0.05), however, no apoptosis was detected in the MDA-MB-23 1 cells after treatment of ADM at any time pint. Conclusion With different molecular and biological characteristics, different br east cancer lines are different in chemosensitivity and drug-resistance, which are related to their apoptotic abilities induced by chemotherapeutic drugs.更多还原