{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Zeng X"],"funding":["Anti-infective Agent Creation Engineering Research Centre of Sichuan Province Fund","Affiliated Hospital of North Sichuan Medical College Plan Projects","Nanchong City and School Cooperation Project"],"pagination":["e70059"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12949608"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["20(1)"],"pubmed_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 "],"journal":["IET systems biology"],"pubmed_title":["Pan-Cancer Analysis of CLDN3 and Its Contribution to 5-FU Resistance in Colorectal Cancer."],"pmcid":["PMC12949608"],"funding_grant_id":["2022JB006","2021YS009","22SXQT0346","KGR202404","20SXQT0101"],"pubmed_authors":["Yang G","Chen Q","Han B","Zeng X","Feng D","Zhang L","Zeng Y"],"additional_accession":[]},"is_claimable":false,"name":"Pan-Cancer Analysis of CLDN3 and Its Contribution to 5-FU Resistance in Colorectal Cancer.","description":"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 ","dates":{"release":"2026-01-01T00:00:00Z","publication":"2026 Jan-Dec","modification":"2026-07-16T23:25:37.636Z","creation":"2026-07-12T03:11:21.158Z"},"accession":"S-EPMC12949608","cross_references":{"pubmed":["41762617"],"doi":["10.1049/syb2.70059"]}}