Cell adhesion molecule 2 (CADM2) promotes brain metastasis by inducing epithelial-mesenchymal transition (EMT) in human non-small cell lung cancer.

Abstract

BackgroundTo investigate the effect of CADM2 on brain metastasis in non-small cell lung cancer (NSCLC).MethodsHuman transcriptome-wide microarray analysis was used to identify gene expression in lung tissue of NSCLC patients with or without brain metastasis, which indicated that CADM2 was significantly up-regulated. Quantitative real-time PCR (qRT-PCR) was used to confirm the CADM2 up-regulation further. SiRNA was used to knock down the expression of CADM2 in NSCLC cell lines and a Transwell assay was performed to determine the effects of CADM2 knockdown on cell migration and invasion. The expressions of Vimentin and E-cadherin were detected by western blot assay.ResultsThe result of microarray analysis and qRT-PCR showed that CADM2 was significantly up-regulated in NSCLC patients with brain metastasis than in those without brain metastasis. The result of the Transwell assay showed that the migration and invasion abilities of NSCLC cells were inhibited after CADM2 knockdown. Also, the expression of Vimentin was reduced while E-cadherin was increased, followed by CADM2 knockdown.ConclusionsThe results showed that CADM2 might promote brain metastasis by inducing epithelial-mesenchymal transition (EMT) in human NSCLC. We propose that CADM2 can be used as a novel molecular target for the prevention and treatment in NSCLC with brain metastasis patients.