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ARID1A , encoding a subunit of SWI/SNF chromatin remodeling complex, is widely recognized as a tumor suppressor gene in multiple tumor types including liver cancer. Previous studies have demonstrated that  ARID1A  deficiency can cause liver cancer metastasis, possibly due to the altered chromatin organization, however the underlying mechanisms remain poorly understood. To address the effect of  Arid1a  deficiency on chromatin organization, we generated chromatin interaction matrices, and exploited the conformation changes upon  Arid1a  depletion in hepatocytes. Our results demonstrated that  Arid1a  deficiency induced A/B compartment switching, topologically associated domain (TAD) remodeling, and decrease of chromatin loops. Further mechanism studies revealed that ATPase BRG1 of SWI/SNF complex could physically interact with RAD21, a structural subunit of chromatin architectural element cohesin; whereas  ARID1A  deficiency significantly diminished the coupled BRG1-RAD21. Interestingly, the tumor-associated genes within the switched compartments were differentially expressed depending upon  Arid1a  depletion or not. As a consequence of  ARID1A  deficiency-induced conformational alteration, the dysregulation of some genes such as  PMP22  and  GSC , promoted the invasion capacity of liver cancer cells. This study provides an insight into liver cancer tumorigenesis and progression related to  ARID1A  mutations.

ARID1A deficiency weakens BRG1-RAD21 interaction that jeopardizes chromatin compactness and drives liver cancer cell metastasis