{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["21(8)"],"submitter":["Wang J"],"pubmed_abstract":["The presence of tumor-associated macrophages (TAMs) characterized by an M2-like phenotype sustains a robust immunosuppressive tumor microenvironment (TME), promoting liver hepatocellular carcinoma (LIHC) progression. Here, we find that genetic deletion of cyclophilin J (CYPJ) in mice significantly accelerates the development of liver cancer. Analysis of immune cell infiltration reveals that high expression of CYPJ correlates with an increased proportion of M1-polarized, anti-tumor macrophages and CD8<sup>+</sup> T cells in the TME. Mechanistically, we demonstrate that CYPJ interacts with AKT1 and inhibits the PI3K-AKT signaling pathway, which leads to polarization of TAMs toward the anti-tumor M1 phenotype, resulting in a tumor-suppressive effect. Collectively, our findings implicate CYPJ "],"journal":["International journal of biological sciences"],"pagination":["3776-3790"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12160919"],"repository":["biostudies-literature"],"pubmed_title":["Cyclophilin J Reprograms Tumor-associated Macrophages to Exert an Anti-tumor Effect in Liver Cancer."],"pmcid":["PMC12160919"],"pubmed_authors":["Zeng Q","Yao C","Fu L","Peng L","Zhang S","Chen S","Sheng C","Wang J","Mao Y"],"additional_accession":[]},"is_claimable":false,"name":"Cyclophilin J Reprograms Tumor-associated Macrophages to Exert an Anti-tumor Effect in Liver Cancer.","description":"The presence of tumor-associated macrophages (TAMs) characterized by an M2-like phenotype sustains a robust immunosuppressive tumor microenvironment (TME), promoting liver hepatocellular carcinoma (LIHC) progression. Here, we find that genetic deletion of cyclophilin J (CYPJ) in mice significantly accelerates the development of liver cancer. Analysis of immune cell infiltration reveals that high expression of CYPJ correlates with an increased proportion of M1-polarized, anti-tumor macrophages and CD8<sup>+</sup> T cells in the TME. Mechanistically, we demonstrate that CYPJ interacts with AKT1 and inhibits the PI3K-AKT signaling pathway, which leads to polarization of TAMs toward the anti-tumor M1 phenotype, resulting in a tumor-suppressive effect. Collectively, our findings implicate CYPJ ","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025","modification":"2026-07-15T06:19:52.495Z","creation":"2026-06-30T03:21:06.959Z"},"accession":"S-EPMC12160919","cross_references":{"pubmed":["40520002"],"doi":["10.7150/ijbs.113197"]}}