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目的探讨X连锁凋亡抑制蛋白(XIAP)抑制剂蒽贝素抑制人胰腺癌细胞Mia PaCa-2凋亡的作用及其可能机制。方法 MTT法和流式细胞术检测不同剂量蒽贝素对Mia PaCa-2细胞增殖和凋亡的影响;RT-PCR法对蒽贝素处理前后Mia PaCa-2细胞中XIAP基因的表达进行检测。Western blotting方法检测蒽贝素作用后细胞XIAP、Caspase 3、促凋亡蛋白Bax和抗凋亡蛋白Bcl-2表达的变化。结果蒽贝素对人胰腺癌细胞增殖具有显著抑制作用(P<0.05),经不同剂量蒽贝素处理后Mia PaCa-2细胞凋亡率明显增高,与未处理组比较差异具有显著性(P<0.01);RT-PCR显示对照组细胞中XIAP的-△△CT值是实验组的11.31倍;经蒽贝素作用24 h后,Mia PaCa-2细胞出现Caspase 3裂解片段,且Bax/Bcl-2比值增大。结论蒽贝素在体外可显著抑制Mia PaCa-2细胞增殖,诱导细胞凋亡,其机制可能是通过拮抗XIAP的作用,激活Caspase相关性的细胞凋亡内源性途径而诱导人胰腺癌细胞发生凋亡。
Objective To investigate the effect and possible mechanism of anthracycline X inhibitor of X chain inhibitor of apoptosis on human pancreatic cancer cell line Mia PaCa-2. Methods The effect of different doses of anthracycline on the proliferation and apoptosis of Mia PaCa-2 cells was detected by MTT assay and flow cytometry. The expression of XIAP gene in Mia PaCa-2 cells was detected by RT-PCR. Western blotting was used to detect the changes of XIAP, Caspase 3, Bax and anti-apoptotic protein Bcl-2 in the cells treated with anthracycline. Results Anthracycline significantly inhibited the proliferation of human pancreatic cancer cells (P <0.05). The apoptosis rate of Mia PaCa-2 cells was significantly increased after treated with different doses of anthracycline (P <0.05), and the difference was significant compared with untreated group <0.01). RT-PCR showed that the -ΔΔCT value of XIAP in control cells was 11.31 times that of the experimental group. Caspase 3 fragment appeared in Mia PaCa-2 cells after treated with anthracycline for 24 h, and the Bax / Bcl -2 ratio increases. CONCLUSION: Anthracycline can significantly inhibit the proliferation of Mia PaCa-2 cells and induce apoptosis in vitro. The possible mechanism is that anthracycline can induce apoptosis of human pancreatic cancer cells by antagonizing the action of XIAP and activating the caspase-related endogenous apoptosis pathway Apoptosis.