Id-1 promotes migration and invasion of non-small cell lung cancer cells through activating NF-κB signaling pathway

Background: numerous studies have shown that id-1 (inhibitor of differentiation 1) is upregulated in several cancers and associated with tumor malignant characters. however,the clinical significance and biological role of id-1 in non-small cell lung cancer (nsclc) remains unclear. methods: we used rt-pcr,western blot and immunohistochemistry to measure id-1 expression in nsclc tissues and matched adjacent noncancerous tissues. the expression pattern of id-1 in nsclc tissues was determined by scoring system of immunohistochemical analysis. the kaplan-meier method was used to calculate the survival curve,and log-rank test to determine statistical significance. the id-1 gene was overexpressed or downreuglated with lentiviral vectors in nsclc cells. and,the migration ability of nsclc cells was tested in a transwell boyden chamber. results: we found that id-1 is generally expressed higher in nsclc tissues compared with matched adjacent noncancerous tissues. we also found that high id-1 expression in tumor tissues is significantly correlated with tumor progression and poor survival in nsclc patients. furthermore,our experimental data revealed that knockdown of id-1 significantly suppressed the proliferation,migration and invasion of nsclc cells,whereas ectopic expression of id-1 promoted the malignant phenotype of nsclc cells. mechanistic study showed that nf-κb signaling pathway contributed to the effects of id-1 in nsclc cells. moreover,blocking the nf-κb pathway significantly inhibited the tumor-promoting actions of id-1 in nsclc cells. conclusions: we identified a tumorigenic role of id-1 in nsclc and provided a novel therapeutic target for nsclc patients. © 2017 the author(s).