This report provides supportive evidence that BRG1 and BRM act as tumor suppressor proteins and implicates a role for their loss in the development of non-small cell lung cancers.

BRM and BRG1 participate in two distinct chromosome remodeling complexes that are functionally complementary in non-small cell lung cancer

Somatic point mutations of the BRG1 gene are present in a small subset of lung tumors

Somatic point mutations of the SMARCA4 gene are present in a small subset of lung tumors.

transcriptional activation of ZNF185 and CYP3A4 is mediated by direct association of BRG1 with their promoters and a decreased level of ZNF185 is a common feature of lung tumours

The BRG1 gene is recurrently inactivated in non small cell lung cancer. mutations were detected in 24% of the lung cancer cell lines. All mutations were homozygous and most predicted truncated proteins. Alterations at BRG1 always occurred in the absence of MYC amplification, suggesting a common role in lung cancer development.

This manuscript provides consistent demonstration that inactivating mutations at the SMARCA4 gene are commonly found in lung cancer cell lines. These observations provide evidence that SMARCA4 constitutes a tumor suppressor gene important in lung cancer.

alterations at BRG1 always occurred in the absence of MYC amplification, suggesting a common role in lung cancer development. In conclusion, our data strongly support that BRG1 is a bona fide tumor suppressor and a major factor in lung tumorigenesis

Loss of BRG1 expression is associated with lung cancer

Results show that BRG1 regulates the expression of MAX through direct recruitment to the MAX promoter, and that depletion of BRG1 strongly hinders cell growth in small cell lung cancer.

results offer direct evidence that BRG1 attenuation contributes to non-small cell lung cancer aggressiveness by altering nucleosome positioning at a wide range of genes, including key cancer-associated genes

SMARCA4 and SMARCA2 deficiency is observed in 5.1% and 4.8% of non-small cell lung cancer

targeting of BRM in combination with radiotherapy is supposed to improve the therapeutic outcome of lung cancer patients harboring BRG1 mutations.The present study shows that the moderate radioresponsiveness of NSCLC cells with BRG1 mutations can be increased upon BRM depletion that is associated with a prolonged Rad51-foci prevalence at DNA DSBs.

BRG1 Loss Predisposes lung cancers to Replicative Stress and ATR Dependency.

Cytology of SMARCA4-Deficient Thoracic Neoplasms: Comparative Analysis of SMARCA4-Deficient Non-Small Cell lung Carcinomas and SMARCA4-Deficient Thoracic Sarcomas.

SMARCA4/BRG1-Deficient Non-Small Cell lung Carcinomas: A Case Series and Review of the Literature.

transformation and lung tumor progression are greatly affected by loss of BRG1