The multi-subunit ATP-dependent chromatin remodeling complex BAF ('mammalian SWI/SNF complex') regulates DNA accessibility during cell fate transitions and functions as a context-dependent tumor suppressor. SMARCB1, as a one of the component of BAF complex, was first found to be biallelically inactivated in ~98% of all malignant rhabdoid tumors (MRT), aggressive pediatric tumors that can occur cranially or extracranially. To examine the mechanisms through which inactivation of SMARCB1 drives malignant rhabdoid tumorigenesis, we conducted RNAseq studies in BT-12 cells reconstituted with either WT or M4 mutant (an in-frame deletion (185-193D) was identified from tumor patient) SMARCB1. These results indicate that loss of SMARCB1 promotes cell proliferation but also impairs cell adhesion and migration, consistent with the hypothesis that SMARCB1 exerts its tumor suppressive function predominantly by inhibiting proliferation.;	;	We applied the RNA-Seq to provide the transcriptomic profiling of BT-12 cell lines without or with stable expression of SMARCB1. SOURCE: Filippo Giancotti (FGGiancotti@mdanderson.org) - Dr. Giancotti Lab UT MD Anderson Cancer Center

Pluto Bioinformatics

GSE139262: Transcriptomic data of established human AT/RT cell lines BT-12.