{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T08:51:25Z","timestamp":1791276685787,"version":"4.1.0"},"reference-count":48,"publisher":"American Association for the Advancement of Science (AAAS)","funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82372792"],"award-info":[{"award-number":["82372792"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82172694"],"award-info":[{"award-number":["82172694"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82373256"],"award-info":[{"award-number":["82373256"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82503287"],"award-info":[{"award-number":["82503287"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82605326"],"award-info":[{"award-number":["82605326"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["spj.science.org"],"crossmark-restriction":true},"short-container-title":["Cancer Commun"],"published-print":{"date-parts":[[2026,1,1]]},"abstract":"<jats:p>\n                    <jats:bold>Background:<\/jats:bold>\n                    Immune checkpoint inhibitors targeting programmed cell death protein 1 (PD-1) have substantially improved the treatment of multiple cancers; however, only a small proportion of gastric cancer (GC) patients achieve durable clinical benefit. The underlying tumor-intrinsic mechanisms driving resistance to anti-PD-1 therapy remain poorly understood. This study aimed to identify key regulators of immunotherapy resistance in GC and to elucidate their functional and mechanistic roles.\n                    <jats:bold>Methods:<\/jats:bold>\n                    Transcriptomic data from anti-PD-1-responsive and anti-PD-1-resistant GC patients were analyzed and integrated with mouse model data and publicly available single-cell RNA sequencing datasets. Functional experiments, including in\u00a0vitro assays and in\u00a0vivo tumor models, were performed to validate candidate genes and explore their roles in tumor progression and immunotherapy resistance.\n                    <jats:bold>Results:<\/jats:bold>\n                    GULP PTB domain-containing engulfment adaptor 1 (GULP1) was identified as a key driver of resistance to anti-PD-1 therapy in GC. Elevated GULP1 expression was associated with poor prognosis and unfavorable clinical responses to PD-1 blockade. GULP1 promoted GC progression and attenuated the therapeutic efficacy of anti-PD-1 treatment. Functionally, GULP1 facilitated the accumulation and metabolic reprogramming of CD36\n                    <jats:sup>+<\/jats:sup>\n                    programmed death-ligand 1 (PD-L1)\n                    <jats:sup>+<\/jats:sup>\n                    tumor-associated macrophages (TAMs) by shaping a lipid-enriched tumor microenvironment, thereby impairing CD8\n                    <jats:sup>+<\/jats:sup>\n                    T-cell function. Mechanistically, GULP1 promoted insulin-induced gene 2 (INSIG2) palmitoylation through the recruitment of zinc finger DHHC-type palmitoyltransferase 8 (zDHHC8), resulting in sterol regulatory element-binding protein 1 (SREBP1) nuclear translocation and enhanced de novo fatty acid biosynthesis. Importantly, pharmacological inhibition of Gulp1 with glycyrrhizic acid significantly restored sensitivity to anti-PD-1 therapy in\u00a0vivo.\n                    <jats:bold>Conclusions:<\/jats:bold>\n                    Collectively, these findings uncovered a previously unrecognized GULP1\u2013fatty acid\u2013CD36\n                    <jats:sup>+<\/jats:sup>\n                    PD-L1\n                    <jats:sup>+<\/jats:sup>\n                    TAM\u2013CD8\n                    <jats:sup>+<\/jats:sup>\n                    T-cell axis that drove resistance to PD-1 blockade in GC, highlighting GULP1 as a promising therapeutic target and predictive biomarker for immunotherapy responsiveness.\n                  <\/jats:p>","DOI":"10.34133\/cancomm.0054","type":"journal-article","created":{"date-parts":[[2026,8,31]],"date-time":"2026-08-31T09:31:10Z","timestamp":1788168670000},"update-policy":"https:\/\/doi.org\/10.34133\/aaas_crossmark_01","source":"Crossref","is-referenced-by-count":0,"title":["GULP1 Fuels Resistance to PD-1 Blockade through Lipid-Mediated Metabolic Reprogramming of Tumor-Associated Macrophages in Gastric Cancer"],"prefix":"10.34133","volume":"46","author":[{"given":"Zihao","family":"Zhang","sequence":"first","affiliation":[{"name":"Department of General Surgery, Zhongshan Hospital, \rFudan University, Shanghai, P. 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