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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。
Objective To investigate the inhibitory effect and mechanism of doxorubicin (ADM) on human breast cancer cell lines Bcap37 and MDA-MB-231, and to evaluate the therapeutic value of apoptosis on breast cancer. Methods Different concentrations of doxorubicin were applied to Bcap37 and MDA-MB-231. The inhibitory rate was detected by MTT assay. The apoptosis, apoptosis-related molecules Fas, Bcl-2 and mutant p53 were detected by flow cytometry (FCM) Changes in expression. Results Doxorubicin inhibited Bcap37 in a dose-and time-dependent manner. However, the inhibition rate of MDA-MB-231 was low and the dose-time effect was not obvious. Doxorubicin increased the expression of Fas in Bcap37 and decreased the expression of Bcl-2, and apoptosis was observed. The expression of p53, Fas and Bcl-2 did not change obviously when Adriamycin was treated with MDA-MB-231, and no apoptotic cells were found. Conclusion Different breast cancer cell lines have different chemosensitivity and drug resistance due to their different molecular biological characteristics. They are related to the difference of chemotherapeutic drugs in inducing apoptosis and provide experimental basis for individualized treatment of breast cancer.