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Radiotherapy is the main component of LC treatment; however, its efficacy is often limited by radioresistance development, resulting in unsatisfactory clinical outcomes. Here, we found\u00a0that LC radiosensitivity is up\u2010regulated by decreased expression of long\u2010chain acyl\u2010CoA synthase 6 (ACSL6) after irradiation. Deletion of ACSL6 results in significant elevation of Friend leukemia integration 1 transcription factor (FLI1) and a marked decline of collagens (COLs). Blocking of ACSL6 impairs the tumor growth and upregulates FLI1, which reduces the levels of COLs and compromises irradiation\u2010induced autophagy, leading to considerable therapeutic benefits during radiotherapy. Moreover, the direct interaction between ACSL6 and FLI1 and engagement between FLI1 and COLs indicates the involvement of the ACSL6\u2010FLI1\u2010COL axis. Finally, the potently adjusted autophagy flux reduces its otherwise contributive capability in surviving irradiation stress and leads to satisfactory radiosensitization for LC radiotherapy. These results demonstrate that enhanced ACSL6 expression promotes the aggressive performance of irradiated LC through increased FLI1\u2010COL\u2010mediated autophagy flux. Thus, the ACSL6\u2010FLI1\u2010Col\u2010autophagy axis may be targeted to enhance the radiosensitivity of LC and improve the management of LC in radiotherapy.<\/jats:p>","DOI":"10.1002\/advs.202403202","type":"journal-article","created":{"date-parts":[[2024,8,29]],"date-time":"2024-08-29T07:04:11Z","timestamp":1724915051000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["Blocking ACSL6 Compromises Autophagy via FLI1\u2010Mediated Downregulation of COLs to Radiosensitize Lung Cancer"],"prefix":"10.1002","volume":"11","author":[{"given":"Wen","family":"Ding","sequence":"first","affiliation":[{"name":"Department of Radiation Medicine College of Naval Medicine Naval Medical University  Shanghai 200433 P. R. 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