ArticleScientific reports2026
TNF-α-responsive YAP1 promotes CCL20 expression in colorectal inflammation and cancer.
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Colitis-associated colorectal cancer (CAC) exemplifies how chronic intestinal inflammation can be converted into sustained epithelial programs and a permissive tumor microenvironment, yet the molecular linkage between inflammatory cytokine cues and chemokine outputs remains incompletely defined. Here, we identify a TNF-α-responsive YAP1-CCL20 program in colorectal inflammation and cancer. Across public cohorts and clinical specimens, YAP1 was elevated in ulcerative colitis and colorectal cancer and positively correlated with TNF-α expression. TNF-α increased YAP1 mRNA in both NCM460 and HCT116 cells. In HCT116 cells, TNF-α also increased YAP1 protein abundance and promoted its nuclear accumulation, whereas infliximab attenuated TNF-α-induced YAP1 mRNA and protein upregulation. Transcriptomic profiling following YAP1 silencing highlighted CCL20 among the most markedly downregulated genes. YAP1 gain- and loss-of-function consistently regulated CCL20 expression and secretion, and mechanistic assays demonstrated that YAP1/TEAD activity directly transactivated the CCL20 promoter. Functionally, TNF-α enhanced proliferation, migration, and invasion of colorectal cancer cells, effects that were blunted by YAP1 knockdown; CCL20 overexpression partially rescued the suppressed malignant phenotypes caused by YAP1 silencing. In vivo, verteporfin and/or infliximab ameliorated DSS-induced colitis, accompanied by reduced colonic Yap1 and Ccl20 expression, lower serum CCL20, and diminished mucosal accumulation of CD3⁺ T cells, CD19⁺ B cells, CD11c⁺ dendritic cells, and FOXP3⁺ regulatory T cells. Moreover, combined YAP pathway inhibition and CCL20 knockdown produced the most pronounced suppression of xenograft tumor growth. Together, these findings position CCL20 as a mechanistically defined downstream effector of YAP1 and suggest that a TNF-α-responsive YAP1-CCL20 program contributes to inflammatory chemokine remodeling in colitis and to malignant phenotypes of colorectal cancer cells.
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