{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,28]],"date-time":"2026-08-28T05:17:59Z","timestamp":1787894279601,"version":"build-2784847793"},"reference-count":84,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,8,28]],"date-time":"2026-08-28T00:00:00Z","timestamp":1787875200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Oncol."],"abstract":"<jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>\n                      Chemoradiotherapy (CRT) represents a cornerstone treatment for colorectal cancer (CRC), yet heterogeneous responses to CRT in treatment response remain a major clinical challenge. Increasing evidence suggests that the tumor immune microenvironment (TME) especially intratumoral CD8\n                      <jats:sup>+<\/jats:sup>\n                      T cells plays an important role in determining CRT efficacy; however, the molecular mechanisms linking tumor-derived factors to immune-mediated treatment sensitivity remain poorly understood. Here, we aimed to identify and characterize regulators of CRT response and the underline mechanisms in CRC.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Transcriptomic profiling of rectal cancer cohorts was performed to identify genes associated with CRT response, followed by pathway enrichment analyses to explore potential biological mechanisms. The functional role of interferon-induced protein 44-like (IFI44L) was investigated using\n                      <jats:italic>in vitro<\/jats:italic>\n                      assays and\n                      <jats:italic>in vivo<\/jats:italic>\n                      immunodeficient NSG and immunocompetent BALB\/c mouse models to distinguish tumor cell-autonomous from immune-dependent effects. RNA sequencing, immune infiltration analysis, chemotaxis assays, immunofluorescence staining, and enzyme-linked immunosorbent assays (ELISA) were further performed to elucidate the underlying molecular mechanisms.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      IFI44L is identified as a candidate gene associated with CRT response through multi-cohort transcriptomic analysis. IFI44L overexpression did not directly alter CRC cell proliferation or CRT response\n                      <jats:italic>in vitro<\/jats:italic>\n                      , nor did it affect tumor growth following CRT in immune-deficient NSG mice. In contrast, IFI44L significantly enhanced CRT efficacy in immunocompetent BALB\/c models, suggesting that its sensitizing effect was in an immune-dependent manner. Mechanistically, IFI44L promoted the expression and secretion of the T cell-attracting chemokine CCL5, leading to increased intratumoral CD8\n                      <jats:sup>+<\/jats:sup>\n                      T cell infiltration and enhanced CRT response.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      Our findings identify IFI44L as an immune-dependent regulator of CRT sensitivity in CRC. By promoting CCL5-mediated CD8\n                      <jats:sup>+<\/jats:sup>\n                      T cell recruitment, IFI44L links tumor-intrinsic molecular alterations with antitumor immune responses and may represent a potential biomarker or therapeutic target for improving CRT efficacy.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fonc.2026.1786425","type":"journal-article","created":{"date-parts":[[2026,8,28]],"date-time":"2026-08-28T04:34:02Z","timestamp":1787891642000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["IFI44L modulates chemoradiotherapy sensitivity and CD8+ T cell infiltration in colorectal cancer"],"prefix":"10.3389","volume":"16","author":[{"given":"Linlin","family":"Zheng","sequence":"first","affiliation":[{"name":"State Key Laboratory of Molecular Oncology, Department of Etiology and Carcinogenesis, National Cancer Center\/National Clinical Research Center for Cancer\/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College","place":["Beijing, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mengjie","family":"Li","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Molecular Oncology, Department of Etiology and Carcinogenesis, National Cancer Center\/National Clinical Research Center for Cancer\/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College","place":["Beijing, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ruoqing","family":"Yan","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Molecular Oncology, Department of Etiology and Carcinogenesis, National Cancer Center\/National Clinical Research Center for Cancer\/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College","place":["Beijing, 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