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目的:探讨外源性SIRPα1基因对乳腺癌细胞株MCF-7增殖和凋亡的影响及相关的分子生物学机制。方法:乳腺癌细胞株MCF-7本身不表达SIRPα1,将SIRPα1基因转染入MCF-7,用EGF刺激,Western blot法检测JNK蛋白及磷酸化的JNK蛋白表达水平的变化,MTT法检测细胞的增殖活性,TUNEL法检测细胞凋亡水平。结果:转染SIRPα1基因后,JNK蛋白的总量没有发生变化,而磷酸化的JNK减少,同时细胞增殖受抑,凋亡增加。SIRPα1胞内段的酪氨酸残基可被多种有丝分裂原活化而发生磷酸化。用EGF刺激转染SIRPα1质粒的MCF-7细胞,与未加刺激的相比,细胞凋亡无明显变化。结论:SIRPα1能促进乳腺癌细胞凋亡,抑制细胞增殖,是一种候选的抑癌基因。
Objective: To investigate the effects of exogenous SIRPα1 gene on proliferation and apoptosis of breast cancer cell line MCF-7 and related molecular mechanisms. Methods: The breast cancer cell line MCF-7 did not express SIRPα1 itself. The SIRPα1 gene was transfected into MCF-7 cells. The expression of JNK protein and phosphorylated JNK protein was detected by Western blot and MTT assay Proliferation activity, TUNEL assay of apoptosis levels. Results: After transfection of SIRPα1 gene, the total amount of JNK protein did not change, while the phosphorylation of JNK decreased while cell proliferation was inhibited and apoptosis increased. Tyrosine residues in the intracellular segment of SIRPα1 are phosphorylated by a variety of mitogen activators. Stimulation of SIRPα1 plasmid with MCF-7 cells by EGF did not show significant changes in apoptosis compared with those without stimulation. Conclusion: SIRPα1 can promote breast cancer cell apoptosis and inhibit cell proliferation, which is a candidate tumor suppressor gene.