ARID1A deficiency weakens BRG1-RAD21 interaction that jeopardizes chromatin compactness and drives HCC metastasis [ChIP-seq]
ARID1A, encoding a subunit of SWI/SNF chromatin remodeling complex, is widely recognized as a tumor suppressor gene in multiple tumor types including hepatocellular carcinoma (HCC). Previous studies have demonstrated that ARID1A deficiency can cause HCC metastasis, possibly due to the altered chromatin organization, however the underlying mechanisms of which remain poorly understood. Whether and how SWI/SNF complex could function as an architectural cooperator to synergistically stabilize chromatin organization should be explored, particular in tumorigenesis. Here we reveal that SWI/SNF complex acts as a potential architectural cooperator via BRG1-RAD21 axis for chromatin organization maintenance; ARID1A deficiency weakens the interaction and thus loosens chromatin compactness, which drives HCC metastasis dependent on the conformational dysregulation on some key genes. Overall design: ChIP-sequencing on AB17 mouse hepatocytes with Ad-GFP (Wild type, WT) and Ad-Cre (Knockout, KO, Arid1a-/-) infection.