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ARID1B loss remodels the chromatin landscape to promote sorafenib resistance in hepatocellular carcinoma

ABSTRACT: CUT&RUN in HepG2 and HLF HCC cell lines mapping H3K27ac, H3K4me3, ARID1B, FOXA1, FOXA2 occupancy under sorafenib treatment and ARID1B-KO conditions. 2x2 factorial (genotype x treatment), 2 biological replicates per condition. Identifies cBAF-pioneer factor chromatin axis mediating sorafenib sensitivity. Preprint: https://doi.org/10.64898/2026.06.11.731725

ORGANISM(S): Homo sapiens

PROVIDER: GSE335770 | GEO | 2026/06/19

REPOSITORIES: GEO

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ARID1B loss drives sorafenib resistance through transcriptional reprogramming in hepatocellular carcinoma

Project description:mRNA-seq was performed in HepG2 hepatocellular carcinoma cells to characterize transcriptional changes driven by ARID1B loss under sorafenib treatment. Wild-type (WT) and ARID1B-knockout (ARID1B-KO) HepG2 cells were treated with sorafenib (5 µM, 48 h) or DMSO vehicle, with three biological replicates per condition. DESeq2 interaction model identified ARID1B-dependent transcriptional responses to sorafenib. Preprint: https://doi.org/10.64898/2026.06.11.731725

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Pooled CRISPR/Cas9 screen identifies chromatin regulatory genes mediating sorafenib resistance in HepG2 hepatocellular carcinoma cells

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ARID1B

Project description:ARID1B

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Inability to switch from ARID1A-BAF to ARID1B-BAF impairs exit from pluripotency and commitment towards neural crest formation in ARID1B-related neurodevelopmental disorders

Project description:The BAF complex modulates chromatin accessibility. Specific BAF configurations have functional consequences, and subunit switches are essential for cell differentiation. ARID1B and its paralog ARID1A encode for mutually exclusive BAF subunits. De novo ARID1B haploinsufficient mutations cause a neurodevelopmental disorder spectrum, including Coffin-Siris syndrome, which is characterized by neurological and craniofacial features. Here, we reprogrammed ARID1B+/- Coffin-Siris patient-derived skin fibroblasts into iPSCs, and modeled cranial neural crest cell (CNCC) formation. We discovered that ARID1B is active only during the first stage of this process, coinciding with neuroectoderm specification, where it is part of a lineage-specific BAF configuration (ARID1B-BAF), including SMARCA4, and nine additional subunits. ARID1B-BAF acts as a gate-keeper, ensuring exit from pluripotency and lineage commitment, by attenuating NANOG, SOX2 and the thousands of enhancers directly regulated by these two pluripotency factors at the iPSC stage. In iPSCs, these enhancers are maintained active by an ARID1A-containing BAF. At the onset of differentiation, cells transition from ARID1A-BAF to ARID1B-BAF, eliciting attenuation of the NANOG/SOX2 networks, and triggering pluripotency exit. Coffin-Siris patient cells fail to perform the ARID1A/ARID1B switch, and maintain ARID1A-BAF at pluripotency enhancers throughout all stages of CNCC formation. This leads to a persistent and aberrant SOX2 and NANOG activity, which impairs CNCC formation. In fact, despite showing the typical neural crest signature (TFAP2A+, SOX9+), the ARID1B-haploinsufficient CNCCs are also NANOG-positive, in stark contrast with the ARID1B-wt CNCCs, which are NANOG-negative. These findings suggest a connection between ARID1B mutations, neuroectoderm formation, and a pathogenic mechanism for Coffin-Siris syndrome.

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Project description:Arid1b ChIP-seq

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Project description:Arid1b ChIP-seq

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RNA-seq analysis upon ARID1B overexpression

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2016-11-12 | GSE75291 | GEO

RNA-seq analysis of primarily cultured neurospheres from ARID1B haploinsufficient and control mice

Project description:To identify ARID1B associated genes in development of neural progenitor , we carried out RNA-seq gene expression profiling analysis in primarily cultured neurospheres from ARID1B haploinsufficient and control mice. 3 biological independent sample from ARID1B hi (hGAFPCre+;ARID1B flox/+) mice were compared with 2 independent litermate control (hGAFPCre+; ARID1B +/+) samples.

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Project description:Sorafenib resistance up-regulated circRNA_104797 could be transmitted by exosomes and responsible for the spread of Sorafenib resistance among HCC cells. CircRNA_104797 was critical for Sorafenib resistance maintenance and silencing circRNA_104797 could substantially increase the efficacy of Sorafenib by inducing apoptosis. Mechanism dissection unveiled that circRNA_104797 could specifically sponge miR-103a-2-5p and miR-660-3p and act as a competing endogenous RNA (ceRNA), thus competitively activated wnt/β-catenin pathway and induced Sorafenib resistance. Meanwhile, LC-MS/MS also revealed that circRNA_104797 could specifically bind to translation related proteins, which might regulate downstream glycan biosynthesis and lipid metabolism, and finally induce Sorafenib resistance. In vivo experiments portrayed a promising clinical application by locally injection of in vivo-grade siRNA for circRNA_104797 by TACE or other manners, which could intensively enhance Sorafenib efficacy in HCC patients. The clinical application of in vivo-grade siRNA for circRNA_104797 in Sorafenib treated HCC patients might shed bright future for the management of advanced HCC.

2020-07-25 | GSE101850 | GEO

RNA-seq transcriptonal profiling in whole hippocampus in WT and Arid1b+/- mice

Project description:There is growing evidence for the involvement of ARID1B, a SWI/SNF ATP-dependent chromatin remodeling subunit, in a broad range of human disorders. Sequencing studies have recurrently implicated ARID1B haploinsufficiency in autism spectrum disorder (ASD), non-syndromic intellectual disability (ID), corpus callosum agenesis, and short stature. In addition, ARID1B is by far the most common cause of Coffin-Siris Syndrome (CSS), a monogenic developmental delay syndrome characterized by a combination of the neuropsychiatric and physical abnormalities mentioned above. To understand how ARID1B mutations lead to these phenotypes, we generated Arid1b mutant mice, which exhibited physical manifestations of developmental delay and behaviors reminiscent of ASD. In the brain, Arid1b haploinsufficiency resulted in changes in the expression of SWI/SNF- regulated genes implicated in ASD.

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