ArticleIET systems biology
Pan-Cancer Analysis of CLDN3 and Its Contribution to 5-FU Resistance in Colorectal Cancer.
Article in IET systems biology. 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Authors and funding
7 authors.
Funding
Abstract
The expression patterns and potential regulatory correlates of CLDN3 in cancers remain insufficiently characterised, necessitating further investigation. We employed R software alongside bioinformatics platforms to analyse the aberrant expression of CLDN3. Experiments in vitro, including proliferation, wound healing, cell cycle progression and apoptosis assays, were conducted to evaluate the role of CLDN3 in CRC. Co-immunoprecipitation (CO-IP) and immunofluorescence analyses were conducted to investigate the interaction between CLDN3 and TRIM28. Western blotting was employed to evaluate the effect of TRIM28 on CLDN3 SUMOylation and protein stability. CLDN3 was found to be overexpressed in several cancers. Genomic alterations and promoter hypomethylation were identified as key contributors to CLDN3 dysregulation. Bioinformatic analysis suggests that CLDN3 is associated with tumour progression and poor prognosis by influencing pathways, it also contributes to immune dysregulation and chemo-resistance mechanisms. Knockdown of CLDN3 in CRC cells decreased proliferation and migration. CLDN3 overexpression was shown to reduce the sensitivity to 5-FU in CRC cells. CO-IP and immunofluorescence confirmed a direct interaction between CLDN3 and TRIM28. Western blot analysis demonstrated that TRIM28 mediates CLDN3 SUMOylation and degradation. CLDN3 influences the growth and chemotherapy resistance of CRC cells, its interaction with TRIM28 makes the TRIM28/CLDN3 axis as a promising therapeutic target for CRC.
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