Claudin Family Participates in the Pathogenesis of Inflammatory Bowel Diseases and Colitis-Associated Colorectal Cancer

Abstract

Claudins are a multigene transmembrane protein family comprising at least 27 members. In gastrointestinal tract, claudins are mainly located in the intestinal epithelia; many types of claudins form a network of strands in tight junction plaques within the intercellular space of neighboring epithelial cells and build paracellular selective channels, while others act as signaling proteins and mediates cell behaviors. Claudin dysfunction may contribute to epithelial permeation disorder and multiple intestinal diseases. Over recent years, the importance of claudins in the pathogenesis of inflammatory bowel diseases (IBD) has gained focus and is being investigated. This review analyzes the expression pattern and regulatory mechanism of claudins based on existing evidence and elucidates the fact that claudin dysregulation correlates with increased intestinal permeability, sustained activation of inflammation, epithelial-to-mesenchymal transition (EMT), and tumor progression in IBD as well as consequent colitis-associated colorectal cancer (CAC), possibly shedding new light on further etiologic research and clinical treatments.

Prognostic value of the post-operative red blood cell distribution width in patients with rectal cancer with neoadjuvant chemoradiation followed by surgery

“…Surgery is the current treatment for solid tumor include rectal cancer. Several studies have reported that the negative effects of postoperative inflammation on prognosis in patients with colorectal cancer [23]. We have also demonstrated that post-operative LMR was closely related to the rectal cancer prognosis by multivariate regression analysis.…”

Pioglitazone Attenuates Experimental Colitis-Associated Hyperalgesia through Improving the Intestinal Barrier Dysfunction

“…Tight junctions are pivotal in regulating intestinal permeability and maintaining intestinal barrier integrity. Emerging evidences from experimental intestinal inflammation models have supported the idea that a strong connection exists between tight junction protein impairment and intestinal inflammation [11,13].…”

STAT3 Signalling via the IL-6ST/gp130 Cytokine Receptor Promotes Epithelial Integrity and Intestinal Barrier Function during DSS-Induced Colitis

“…The claudin family of proteins constitutes the tight junctions between adjacent IECs to regulate passage of ions, molecules, and barrier permeability. Shifts in the expression of tight junction proteins can result in barrier dysfunction and invasion of pathogenic bacteria across the intestinal epithelium, which are associated with the pathogenesis of IBD [28][29][30]. While previous studies have demonstrated that the STAT3 activators IL-6 and IL-22 can regulate the expression of claudin 2 to regulate intestinal permeability in vitro [31][32][33], whether this effect is observed in vivo is yet to be investigated.…”