Fig. 3

The mechanism by which the ARID1A variation contributes to the pathogenesis of CRCs. ARID1A, a subunit of the chromatin remodeling protein SWI/SNF, is considered to be associated with the tumorigenesis and the progression of CRCs. The process is initiated by the mutation of multiple genes (i.e., TP53, ARID domain-containing gene family, APC, FBXW7, PIK3CA, PD-L1, and KRAS), the dysregulation of several signaling pathways (i.e., PI3K/Akt signaling, MEK/ERK pathway, WNT pathway, AURKA-mediated signaling, and DNA repair pathways), chromatin remodeling, mismatch repair deficiency, and DNA hypermethylation, leading to the cell cycle arrest, proliferation, and survival of the CRC cells. ARID1A AT-rich interaction domain 1A, APC adenomatous polyposis coli, FBXW7 F-Box and WD repeat domain containing 7, PIK3CA phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit α, SWI/SNF SWItch/Sucrose non-fermenting, PD-L1 programmed death ligand 1, KRAS Kirsten rat sarcoma viral oncogene homolog, AURKA aurora kinase A