{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Xu G"],"funding":["Natural Science Foundation of Tianjin Municipal Science and Technology Commission","Natural Science Foundation of Tianjin Municipal Science and Technology Commission (Natural Science Foundation of Tianjin Municipal Science & Technology Commission)","National Natural Science Foundation of China","National Natural Science Foundation of China (National Science Foundation of China)"],"pagination":["888"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9587286"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["13(10)"],"pubmed_abstract":["Histone deacetylase 6 (HDAC6), a member of the HDAC family, has been identified as a potential therapeutic target for tumor therapy, but the function and underlying mechanisms of HDAC6 in colon cancer are incompletely characterized. Our study showed that the infiltration ratio of M2 macrophages was increased in colon cancer tissues with high HDAC6 expression. Similarly, the knockdown of HDAC6 in colon cancer cells inhibited cocultured macrophage M2 polarization in vitro. Analysis of the antibody chip revealed that HDAC6 promoted sIL-6R release to enhance macrophage M2 polarization. Mass spectrometry and immunoprecipitation demonstrated that, mechanistically, HDAC6 interacted with transforming growth factor β-activated kinase 1 (TAK1), deacetylated TAK1 at T178 and promoted TAK1 phosphoryla"],"journal":["Cell death & disease"],"pubmed_title":["HDAC6-dependent deacetylation of TAK1 enhances sIL-6R release to promote macrophage M2 polarization in colon cancer."],"pmcid":["PMC9587286"],"funding_grant_id":["82171728","20JCQNJC00130"],"pubmed_authors":["Yang G","Li H","Yao Y","Wang S","Zhao G","Niu L","Zhu X","Wang Y","Xu G"],"additional_accession":[]},"is_claimable":false,"name":"HDAC6-dependent deacetylation of TAK1 enhances sIL-6R release to promote macrophage M2 polarization in colon cancer.","description":"Histone deacetylase 6 (HDAC6), a member of the HDAC family, has been identified as a potential therapeutic target for tumor therapy, but the function and underlying mechanisms of HDAC6 in colon cancer are incompletely characterized. Our study showed that the infiltration ratio of M2 macrophages was increased in colon cancer tissues with high HDAC6 expression. Similarly, the knockdown of HDAC6 in colon cancer cells inhibited cocultured macrophage M2 polarization in vitro. Analysis of the antibody chip revealed that HDAC6 promoted sIL-6R release to enhance macrophage M2 polarization. Mass spectrometry and immunoprecipitation demonstrated that, mechanistically, HDAC6 interacted with transforming growth factor β-activated kinase 1 (TAK1), deacetylated TAK1 at T178 and promoted TAK1 phosphoryla","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Oct","modification":"2025-04-26T00:53:25.582Z","creation":"2025-04-06T09:55:29.976Z"},"accession":"S-EPMC9587286","cross_references":{"pubmed":["36270986"],"doi":["10.1038/s41419-022-05335-1"]}}