Loss of BRMS1 promotes a mesenchymal phenotype through regulation of Twist1

Analysis of BRMS1 KD-induced EMT in non-samll cell lung cancer at gene expression level. The hypothesis tested in the present study was that BRMS1 KD induces EMT through differential regulation of EMT genes and Twist1 KD restores the epithelial phenotype in cells with BRMS1 KD. Results provide important information of biological functions in lung cancer which BRMS1 KD involves in, such as EMT, signaling, biological adhesion, immune system process, response to stimulus, and so on. Total RNA obtained from NSCLC H1993 cells infected with lentivirus encoding shRNA BRMS1 or shRNA BRMS1/shRNA Twist1, compared to shRNA control sequence. Illumina microarry were performed using Human HT-12 in duplicates.