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ARID1A deficiency weakens BRG1-RAD21 interaction that jeopardizes chromatin compactness and drives liver cancer cell metastasis
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ARID1A deficiency weakens BRG1-RAD21 interaction that jeopardizes chromatin compactness and drives liver cancer cell metastasis
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ARID1A deficiency weakens BRG1-RAD21 interaction that jeopardizes chromatin compactness and drives liver cancer cell metastasis
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Journal Article
ARID1A deficiency weakens BRG1-RAD21 interaction that jeopardizes chromatin compactness and drives liver cancer cell metastasis
2021
Overview
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.
Publisher
Nature Publishing Group UK,Springer Nature B.V,Nature Publishing Group
Subject
/ 13/109
/ 13/51
/ 14/19
/ 38/39
/ 38/91
/ 45
/ 45/23
/ 64/60
/ 82/80
/ Animals
/ Biomedical and Life Sciences
/ Chromatin Assembly and Disassembly - genetics
/ Cohesin
/ DNA-Binding Proteins - deficiency
/ Humans
/ Mice
/ Nuclear Proteins - metabolism
/ Peripheral myelin protein 22
/ Transcription Factors - deficiency
