{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,14]],"date-time":"2026-10-14T19:03:43Z","timestamp":1792004623462,"version":"4.4.0"},"reference-count":51,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2026,8,12]],"date-time":"2026-08-12T00:00:00Z","timestamp":1786492800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2026,8,12]],"date-time":"2026-08-12T00:00:00Z","timestamp":1786492800000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J of Gastro and Hepatol"],"published-print":{"date-parts":[[2026,9]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Colorectal cancer (CRC) is a major global health burden. While immune checkpoint inhibitors have greatly advanced cancer therapy, their therapeutic effects are unsatisfactory in microsatellite\u2010stable\/proficient mismatch repair CRC. This study explored the molecular mechanisms underlying CRC immune evasion.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Bioinformatics analysis and machine learning were applied to screen key targets. Real\u2010time quantitative polymerase chain reaction (RT\u2010PCR) detected CCT2 and programmed cell death ligand 1 (PD\u2010L1) mRNA levels, and Western blot measured PD\u2010L1, STAT3, and p\u2010STAT3 protein expressions. Cell proliferation, apoptosis, invasion, migration, and immune cytotoxicity were assessed via 5\u2010ethynyl\u20102\u2032\u2010deoxyuridine (EdU), TUNEL, Transwell, wound healing, and lactate dehydrogenase (LDH) assays. ELISA was used to detect interferon\u2010\u03b3 (IFN\u2010\u03b3) and tumor necrosis factor\u2010\u03b1 (TNF\u2010\u03b1) secretion, and xenograft mouse models were established for in\u00a0vivo verification, with immunohistochemistry detecting tumor PD\u2010L1 expression.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      This study identified CCT2 as a core gene of CRC. Analysis of public datasets revealed a significant increase in CCT2 expression in CRC tissues. CCT2 knockdown inhibited CRC cell growth, invasiveness, and migration in\u00a0vitro and in\u00a0vivo. A positive correlation between CCT2 and PD\u2010L1 expression was observed in public and clinical CRC patients. Furthermore, CCT2 knockdown promoted the activation and proinflammatory cytokine secretion of CD8\n                      <jats:sup>+<\/jats:sup>\n                      T cells. Mechanistically, CCT2 knockdown diminished PD\u2010L1 expression and promoted activation of CD8\n                      <jats:sup>+<\/jats:sup>\n                      T cells via the JAK1\u2010STAT3 signaling pathway.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>CCT2 upregulation promoted immune escape of colorectal cancer via regulating the JAK1\u2010STAT3\u2010PD\u2010L1 axis, suggesting a promising role of CCT2 in CRC treatment.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/jgh.70617","type":"journal-article","created":{"date-parts":[[2026,8,12]],"date-time":"2026-08-12T09:40:26Z","timestamp":1786527626000},"page":"2795-2808","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["CCT2 Promotes Immune Escape in Colorectal Cancer by Regulating the 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