细胞黏附分子2对非小细胞肺癌增殖、侵袭和凋亡的影响

Effects of cell adhesion molecule 2 on proliferation,invasion and apoptosis of non-small cell lung cancer

目的探究细胞黏附分子2(CADM2)对非小细胞肺癌(non-small cell lung cancer,NSCLC)生物学过程的潜在作用和机制。方法采用实时荧光定量PCR(RT-qPCR)和免疫蛋白印迹法(Western blot)测定CADM2在人正常肺细胞系Gekko lung-1和肺癌细胞系A549和H460中的表达情况。利用过表达技术处理A549和H460细胞,并分为过表达组(pcDNA3.1-CADM2组)、载体对照组(pcDNA3.1-NC组)及未处理组(control组)。转染后,采用细胞计数试剂盒(CCK-8)和Transwell实验检测CADM2对A549和H460细胞增殖及侵袭能力的影响。进一步通过流式细胞术评估CADM2对凋亡率的影响。此外,通过RT-qPCR和Western blot检测CADM2过表达后AKT/mTOR通路蛋白表达的变化情况。结果与正常肺细胞系Gekko lung-1相比,CADM2在肺癌细胞系A549和H460中呈低表达(P<0.05)。与载体对照组及未处理组相比,CADM2过表达组A549和H460细胞增殖和侵袭能力显著降低,细胞凋亡率提高,并且p-AKT和p-mTOR的表达水平明显提升(均P<0.05)。结论CADM2通过调节AKT/mTOR信号通路抑制非小细胞肺癌细胞增殖和侵袭,并且诱导细胞凋亡,提示CADM2是治疗非小细胞肺癌的新型靶点。

Objective To investigate the potential effects and mechanism of cell adhesion molecule 2(CADM2)on non-small cell lung cancer(NSCLC).Methods Real-time fluorescence quantitative PCR(RT-qPCR)and Western blot were used to determine the expression level of CADM2 in human normal lung cell line Gekko lung-1 and lung cancer cell lines A549 and H460.A549 and H460 cells were treated using overexpression vector and divided into three groups:overexpression group(pcDNA3.1-CADM2 group),vector control group(pcDNA3.1-NC group)and untreated group(control group),respectively.After transfection,the impact of CADM2 overexpression on proliferation and invasion of A549 and H460 cells was assessed using cell counting kit-8(CCK-8)and Transwell assay.The effect of CADM2 on the apoptosis rate was measured by flow cytometry.In addition,the expression of AKT/mTOR pathway proteins after CADM2 overexpression was examined by RT-qPCR and Western blot.Results CADM2 was downregulated in NSCLC cell lines A549 and H460 compared with Gekko lung-1 cell line(P<0.05).Compared with vector control group and untreated group,the proliferation and invasion abilities of A549 and H460 cells in CADM2 overexpression group were significantly attenuated,the cell apoptosis rate was increased,and the expression levels of p-AKT and p-mTOR was decreased(P<0.05).Conclusion CADM2 can inhibit the proliferation and invasion of NSCLC cells by regulating AKT/mTOR signaling pathway,and induce the apoptosis,suggesting that CADM2 is a novel target for the treatment of NSCLC.