{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T09:51:21Z","timestamp":1791193881142,"version":"4.1.0"},"reference-count":44,"publisher":"Wiley","license":[{"start":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T00:00:00Z","timestamp":1791158400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T00:00:00Z","timestamp":1791158400000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100025019","name":"Support for Pioneering Research Initiated by the Next Generation","doi-asserted-by":"publisher","award":["JPMJSP2180"],"award-info":[{"award-number":["JPMJSP2180"]}],"id":[{"id":"10.13039\/501100025019","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001700","name":"Ministry of Education, Culture, Sports, Science and Technology","doi-asserted-by":"publisher","award":["JPMXS0120330644"],"award-info":[{"award-number":["JPMXS0120330644"]}],"id":[{"id":"10.13039\/501100001700","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001691","name":"Japan Society for the Promotion of Science","doi-asserted-by":"publisher","award":["25K01589"],"award-info":[{"award-number":["25K01589"]}],"id":[{"id":"10.13039\/501100001691","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["febs.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["FEBS Open Bio"],"abstract":"<jats:p>Quiescent cancer cells (QCCs) drive tumor dormancy and recurrence through their resistance to conventional therapies. Furthermore, because QCCs rely on oxidative phosphorylation and maintain a fragile redox balance, we hypothesized that they harbor a targetable redox vulnerability. Here, we show that the mitochondria\u2010targeted agent dequalinium chloride (DQ) selectively kills QCCs in hypoxia\u2010 and nutrient limitation\u2010induced quiescent models, including H2228 cells, multicellular spheroids, and colorectal cancer organoids, while sparing proliferating cells and normal fibroblasts. DQ induces ROS accumulation beyond the survival threshold of QCCs, leading to lipid peroxidation and ferroptotic cell death, whereas proliferating cells undergo limited caspase\u2010independent apoptosis. These findings highlight redox imbalance as an actionable vulnerability of QCCs and position DQ as a potential repurposed agent for eliminating QCCs.<\/jats:p>","DOI":"10.1002\/2211-5463.70344","type":"journal-article","created":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T08:55:48Z","timestamp":1791190548000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Selective elimination of quiescent cancer cells by dequalinium chloride via\n                    <scp>ROS<\/scp>\n                    \u2010mediated ferroptosis"],"prefix":"10.1002","author":[{"given":"Kotaro","family":"Miyamoto","sequence":"first","affiliation":[{"name":"School of Life Science and Technology Institute of Science Tokyo  Yokohama Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shiori","family":"Sakai","sequence":"additional","affiliation":[{"name":"School of Life Science and Technology Institute of Science Tokyo  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