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Related mechanism diagram. In the combined AOM/DSS-induced CAC mouse model, due to continuous inflammatory stimulation and repeated tissue damage, the WNT pathway was activated. Cdh1 and Ctnnb1 no longer interacted leading to unstable intercellular adhesion junctions, abnormal epithelial proliferation, accelerated tissue repair, dysregulation of cell cycle G1/S restriction point control, and abnormal expression of key regulators Ccnd1 and CDK4.
