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. 2024 May 12;15:159. doi: 10.1007/s12672-024-01019-8

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© The Author(s) 2024

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig.1 — Mechanism of action of MLCK1 and analysis of data from TCGA. a recruitment of MLCK1 to the perijunctional actomyosin ring (PAMR) affects the binding of tight junction-related proteins such as ZO-1, claudins, and then increases the permeability of epithelial tight junctions, thereby causing a reduction in intestinal barrier function. A small molecule named Divertin that MLCK1 recruitment to the PAMR, restores barrier function and prevents disease progression in experimental inflammatory bowel disease caused by pro-inflammatory cytokine such as TNF, INF and et.al. b analysis of data from TCGA showed a significant difference in MLCK1 expression between normal and colorectal cancer patients (p < 0.01). c, d no significant correlation with overall survival (OS) and disease-free survival (DFS)