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Colitis associated cancer (CAC) is the colorectal cancer (CRC) subtype that is associated with bowel disease such as ulcerative colitis (UC). The data on role of NF- κ B signaling in development and progression of CAC were derived from preclinical studies, whereas data from human are rare. The aim of this work was to study the contribution of NF- κ B pathway during UC and CAC, as well as the immunomodulatory effect of all-trans retinoic acid (AtRA). We analyzed the expression of NOS2, TNF- α , TLR4, and NF- κ B, in colonic mucosa. We also studied NO/TNF- α  modulation by LPS in colonic mucosa pretreated with AtRA. A marked increase in TLR4, NF- κ B, TNF- α , and NOS2 expression was reported in colonic mucosa. The relationship between LPS/TLR4 and TNF- α /NO production, as well as the role of NF- κ B signaling, was confirmed by ex vivo experiments and the role of LPS/TLR4 in NOS2/TNF- α  induction through NF- κ B pathway was suggested. AtRA downregulates NOS2 and TNF- α  expression. Collectively, our study indicates that AtRA modulates in situ LPS/TLR4/NF- κ B signaling pathway targeting NOS2 and TNF- α  expression. Therefore, we suggest that AtRA has a potential value in new strategies to improve the current therapy, as well as in the clinical prevention of CAC development and progression.

mediators of inflammation

All-Trans Retinoic Acid Modulates TLR4/NF-<i>κ</i>B Signaling Pathway Targeting TNF-<i>α</i>and Nitric Oxide Synthase 2 Expression in Colonic Mucosa during Ulcerative Colitis and Colitis Associated Cancer

All-Trans Retinoic Acid Modulates TLR4/NF-κB Signaling Pathway Targeting TNF-αand Nitric Oxide Synthase 2 Expression in Colonic Mucosa during Ulcerative Colitis and Colitis Associated Cancer