CD147对肺癌A549细胞增殖、迁移和侵袭的影响

Effects of CD147 on proliferation,migration,and invasion of lung cancer A549 cells

目的:探讨细胞外基质金属蛋白酶诱导因子(extracellular matrix metalloproteinase inducer,EMMPRIN,EMP,又称CD147)对肺癌A549细胞增殖、迁移及侵袭能力的影响及其可能的机制。方法:将CD147过表达慢病毒、短发夹RNA(short hairpin RNA,sh RNA)干扰CD147表达的慢病毒及阴性对照(negative control,NC)慢病毒分别感染肺癌A549细胞,获得CD147稳定过表达的A549EMP细胞、稳定干扰CD147表达的A549sh EMP细胞和阴性对照A549NC细胞。应用CCK-8(cell counting kit-8)法、细胞划痕实验和Transwell小室法分别检测A549EMP、A549sh EMP和A549NC细胞的增殖、迁移及侵袭能力;蛋白质印迹法检测A549EMP、A549sh EMP和A549NC细胞中β-catenin的核表达情况。结果:A549EMP细胞的增殖、迁移和侵袭能力明显高于未进行慢病毒感染的空白对照组A549细胞和阴性对照组A549NC细胞(P<0.05),而A549sh EMP细胞的增殖、迁移和侵袭能力明显低于空白对照组A549细胞和阴性对照组A549NC细胞(P<0.05)。A549EMP细胞β-catenin的核表达水平明显高于空白对照组A549细胞和阴性对照组A549NC细胞(P<0.05),而A549sh EMP细胞β-catenin的核表达水平明显低于空白对照A549细胞和阴性对照组A549NC细胞(P<0.05)。结论:CD147可增强肺癌A549细胞的增殖、迁移和侵袭能力,其机制可能与β-catenin的激活有关。

Objective： To investigate the effects of extracellular matrix metalloproteinase inducer （EMMPRIN, EMP, also known as CD147） on the proliferation, migration, and invasion of lung cancer A549 cells, and to explore its possible mechanism. Hechods： CD147-overexpress control （NC） lentivirus were A549EMP cells with CD147 negative control A549NC ce ion lentivirus, short hairpin RNA （shRNA） lentivirus and negative infected into A549 cells, respectively. The stable clones of overexpression, A549shEMP cells with CD147 silencing, and IIs were obtained, respectively. The abilities of proliferation, migration and invasion of A549EMP, A549shEMP and A549NC cells were measured by cell counting kit-8 （CCK-8）, wound scratch assay and Transwell test, respectively. The expressions of β-catenin in nuclei of A549EMP, A549shEMP and A549NC cells were detected by Western blotting. Results： The abilities of proliferation, migration and invasion of A549EMP cells were higher than those of A549 cells without any infection （as a blank control） and A549NC cells （P 〈 0.05）, but the abilities of proliferation, migration, and invasion of A549shEMP cells were lower （P 〈 0.05）. The expression of 13-catenin in nucleus of A549EMP cells was higher than that of the blank control cells and A549NC cells （P 〈 0.05）; whereas, the expression of β-catenin in nucleus of A549shEMP cells was lower （P 〈 0.05）. Conclusion： CD147 can enhance the abilities of proliferation, migration and invasion of lung cancer A549 cells. This effect may be related to the activation of β-catenin.