Fig. 2

Bioinformatic analysis and in vitro experiments revealed that ARID1A deficiency promotes HCC cell proliferation, migration, and invasion in vitro. a, b GSEA identified that the cell cycle-related E2F pathway was more enriched in the ARID1A normal group. c GSEA identified that the epithelial-mesenchymal transition (EMT) pathway was highly enriched in the ARID1A-deficient group compared with the ARID1A normal functioning group. d The ARID1A-deficient group had higher mesenchymal marker gene expression. e ARID1A CRISPR knockout in Hep3B and SK-HEP-1 cell lines was confirmed by Western blotting. f CCK-8 assays showing cell viability of ARID1A in WT and ARID1A knockout SK-Hep-1 and Hep3B cells (n = 6). g Clone formation of ARID1A knockout Hep3B and SK-HEP-1 cells compared with their controls (n = 3). h Image results of migration and invasion assays of HCC cells between ARID1A knockout and control cells (n = 3). (* P < 0.05, ** P < 0.01, *** P < 0.001), Scale bar = 100 μm