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The acyl\u2010CoA synthetase long\u2010chain (ACSL) family (ACSL1\u2013ACSL6) catalyzes ATP\u2010dependent activation of long\u2010chain fatty acids into acyl\u2010CoA, a bioactive intermediate in lipid synthesis, \u03b2\u2010oxidation, membrane biogenesis, and signal transduction. Dysregulated ACSL expression is widespread in malignancies, but their non\u2010metabolic functions (ferroptosis regulation, tumor immune microenvironment remodeling) and translational potential of targeted therapies remain to be systematically summarized.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>This narrative review comprehensively synthesizes existing literature on the biological functions of ACSL family members in cancer. We retrieved and analyzed studies focusing on ACSL\u2010mediated lipid metabolic reprogramming, ferroptosis modulation, and immunomodulatory effects, with particular emphasis on isoform\u2010specific mechanisms and the context\u2010dependent roles (pro\u2010tumorigenic or tumor\u2010suppressive) of the ACSL family across different cancer types. Additionally, we summarized emerging therapeutic strategies targeting ACSL isoforms and their translational potential.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>ACSL isoforms exert distinct context\u2010dependent effects:ACSL1 promotes immunosuppressive TIME via M2 macrophage polarization;ACSL3\/4 have antagonistic roles in ferroptosis;ACSL5 exerts dual effects via lipid metabolism, apoptosis, and immunity;ACSL6 involves autophagy and hematological malignancies. Dysregulation correlates with tumor progression, drug resistance, and immunotherapy response, while emerging ACSL\u2010targeted drugs show substantial translational potential.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>The ACSL family serves as a key regulatory node integrating lipid metabolism, ferroptosis, and tumor immunity. Its isoform\u2010specific mechanisms and context\u2010dependent characteristics highlight its potential as a precise therapeutic target. Future research should focus on optimizing isoform\u2010selective inhibitors, clarifying their synergistic effects with existing therapies (e.g., immune checkpoint inhibitors, radiotherapy), and validating their translational efficacy through clinical trials to advance the development of innovative cancer treatment strategies.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/ctm2.70643","type":"journal-article","created":{"date-parts":[[2026,3,17]],"date-time":"2026-03-17T10:20:45Z","timestamp":1773742845000},"source":"Crossref","is-referenced-by-count":4,"title":["The multifaceted roles of the ACSL family in cancer: Metabolic reprogramming, ferroptosis regulation and tumour immune microenvironment remodelling"],"prefix":"10.1002","volume":"16","author":[{"given":"Haocai","family":"Li","sequence":"first","affiliation":[{"name":"Hepatic Surgery Center, Clinical Medical Research Center of Hepatic Surgery at Hubei Province Tongji Hospital, Tongji Medical College, Huazhong 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