Dataset Information


Loss of BRMS1 promotes a mesenchymal phenotype through regulation of Twist1

ABSTRACT: 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. Overall design: 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.

INSTRUMENT(S): Illumina HumanHT-12 V4.0 expression beadchip

SUBMITTER: Jeffrey Zhao 

PROVIDER: GSE62359 | GEO | 2014-11-12



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Loss of BRMS1 promotes a mesenchymal phenotype through NF-κB-dependent regulation of Twist1.

Liu Yuan Y   Mayo Marty W MW   Xiao Aizhen A   Hall Emily H EH   Amin Elianna B EB   Kadota Kyuichi K   Adusumilli Prasad S PS   Jones David R DR  

Molecular and cellular biology 20141103 1

Breast cancer metastasis suppressor 1 (BRMS1) is downregulated in non-small cell lung cancer (NSCLC), and its reduction correlates with disease progression. Herein, we investigate the mechanisms through which loss of the BRMS1 gene contributes to epithelial-to-mesenchymal transition (EMT). Using a short hairpin RNA (shRNA) system, we show that loss of BRMS1 promotes basal and transforming growth factor beta-induced EMT in NSCLC cells. NSCLC cells expressing BRMS1 shRNAs (BRMS1 knockdown [BRMS1(K  ...[more]

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