关键词: 富含亮氨酸的α2糖蛋白1, RUNX1/OPN信号, 非小细胞肺癌, 增殖, 迁移侵袭

Abstract: Objective To investigate the regulatory effect of leucine-rich-alpha2-glycoprotein 1(LRG1) on the proliferation,migration and invasion of non-small cell lung cancer(NSCLC) cellsvia the Runt-related transcription factor 1(RUNX1)/osteopontin(OPN) axis. Methods To determin the expression of LRG1,RUNX1 and OPN in cultured human type II alveolar epithelial cells and human NSCLC cell lines A549,NCI-H838 and NCI-H1650.The human NSCLC cell line A549 cultured in vitro was randomly divided into control group,LRG1 knockdown group,negative control group,RUNX1 overexpression group,LRG1 knockdown + RUNX1 overexpression group by random number table method,after cells were grouped and transfected with plasmids,to detect the proliferation,apoptosis,migration,invasion,the expression of apoptosis proteins(Bcl-2,caspase-3,Bax) and epithelial-mesenchymal transition marker proteins(N-cadherin,E-cadherin),the expressions of LRG1,RUNX1 and OPN in A549 cells in each group.〖WTHZ〗Results Compared with human type II alveolar epithelial cells,the mRNA and protein expressions of LRG1,RUNX1 and OPN in human NSCLC cell lines A549,NCI-H838 and NCI-H1650 higher(P<0.05).Compared with the control group,the positive rate of EdU,the migration rate,the number of invasion,the mRNA and protein expressions of LRG1,RUNX1 and OPN,and the protein expression of Bcl-2 and N-cadherin in the LRG1 knockdown group were decreased(P<0.05),and the apoptosis rate and the protein expression of caspase-3,Bax,and E-cadherin were increased(P<0.05);The changes of various indicators in RUNX1 overexpression group were contrary to those in LRG1 knockdown group,and the overexpression of RUNX1 could reverse the effects of LRG1 knockdown on various indicators of cells.Conclusion Knockdown of LRG1 can inhibit the proliferation,migration and invasion of NSCLC cells and promote their apoptosis by down-regulating the expressions of RUNX1 and OPN.

Key words: leucine-rich-alpha2-glycoprotein 1, RUNX1/OPN signaling, non-small cell lung cancer, proliferation, migration and invasion