敲减MAC30通过PI3K/AKT抑制人乳腺癌细胞增殖并诱导其凋亡

Knockdown of MAC30 inhibits proliferation of human breast cancer cells and induces apoptosis of via PI3K/AKT

目的:探讨MAC30在乳腺癌中的作用和机制。方法:使用慢病毒介导的Lenti-shRNA来沉默乳腺癌细胞MCF7和MDA-MB-231中MAC30的表达,并通过Western Blot检测相关蛋白的表达;采用CCK8法检测细胞增殖;Annexin V-FITC/PI双染色法检测细胞凋亡。结果:MAC30的表达下调后乳腺癌细胞的增殖率减少且凋亡率增加,通过Western Blot,发现MAC30敲低后p-AKT,Cyclin D1和Bcl-2的表达明显下降,而BAX的表达增高。结论:敲减MAC30的表达后,可以明显抑制乳腺癌细胞增殖并诱导其凋亡,而MAC30可能是通过PI3K/AKT信号通路来调控乳腺癌的发生发展过程。因此,MAC30可能是一个治疗乳腺癌的潜在治疗靶点。

Objective:To elucidate the role and functional mechanism of action of MAC30 in breast cancer.Methods:Lentiviral-mediated Lenti-shRNA was used to silence the expression of MAC30 in MCF7 and MDA-MB-231 breast cancer cells.The expression of related proteins was detected by Western blotting.Cell proliferation was evaluated by the CCK8 assay and apoptosis was detected by the Annexin V-FITC/PI double staining method.Results:The proliferation of the breast cancer cell sdecreased,and apoptosis increased after downregulation of MAC30.Western blotting also revealed that the expression of p-AKT,Cyclin D1,and Bcl-2 were significantly reduced and the expression of BAX increased after MAC30 knockdown.Conclusion:This study suggested that knocking down MAC30 couldinhibit the proliferation of breast cancer cells and induce their apoptosis.MAC30 may regulate the development of breast cancer through the PI3 K/AKT signaling pathway,and may represent a potential therapeutic target for breast cancer therapy.