VCAN通过PI3K/AKT信号通路调控乳腺癌MDA-MB-231细胞的增殖

VCAN regulating the proliferation of breast cancer MDA-MB-231 cells through the PI3K/AKT signaling pathway

目的探讨多能蛋白聚糖(VCAN)通过PI3K/AKT信号通路对乳腺癌细胞MDA-MB-231增殖的影响。方法利用Western Blot和qRT-PCR检测VCAN在正常人乳腺细胞MCF-10A和三株乳腺癌细胞中的表达水平。选取VCAN高表达细胞株MDA-MB-231为实验对象,实验分组为NC组、siRNA1-VCAN组和siRNA2-VCAN组。采用MTT法及克隆形成法检测转染后的乳腺癌细胞增殖变化。Western Blot检测p-AKT、AKT、p-PI3K、PI3K的蛋白相对表达水平。结果与正常人乳腺细胞相比,VCAN在乳腺癌细胞中的表达量显著上升(P<0.05)。下调VCAN表达量,MDA-MB-231细胞的增殖显著被抑制(P<0.05)。同时,下调VCAN表达量,p-AKT、p-PI3K蛋白水平显著下降(P<0.05)。结论VCAN在乳腺癌MDA-MB-231细胞中,可能通过PI3K/AKT信号通路调控细胞增殖能力。

Objective To investigate the effect of versican(VCAN)on the proliferation of breast cancer cells MDA-MB-231 through the PI3K/AKT signaling pathway.Methods Western Blot and qRT-PCR were used to detect the expression level of VCAN in normal human breast cells MCF-10A and three breast cancer cells.The VCAN high-expressing cell line MDA-MB-231 was selected as the experimental object,a nd they were divided into the NC group,siRNA1-VCAN group,and siRNA2-VCAN group.The MTT method and clone formation method were used to detect the proliferation of breast cancer cells after transfection.Western Blot was used to detect the relative protein expression levels of p-AKT,AKT,p-PI3K and PI3K.Results Compared with that of the normal human breast cells,the expression of VCAN in breast cancer cells increased significantly(P<0.05).When the expression of VCAN was down-regulated,the proliferation of MDA-MB-231 cells was significantly inhibited(P<0.05).At the same time,the expression of VCAN was downregulated,and the protein levels of p-AKT and p-PI3K decreased significantly(P<0.05).Conclusion VCAN may regulate cell proliferation through PI3K/AKT signaling pathway in breast cancer MDA-MB-231 cells.