{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,16]],"date-time":"2026-10-16T08:55:55Z","timestamp":1792140955851,"version":"4.4.0"},"reference-count":44,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2023,2,10]],"date-time":"2023-02-10T00:00:00Z","timestamp":1675987200000},"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. Pharmacol."],"abstract":"<jats:p>Metabolic adaptation is an emerging hallmark of tumors. <jats:italic>De novo<\/jats:italic> fatty acid synthesis is an important metabolic process to produce metabolic intermediates for energy storage, biosynthesis of membrane lipids and generation of signaling molecules. Acetyl-CoA carboxylase 1 (ACC1) is a critical enzyme in the fatty acid synthesis, which carboxylates acetyl-CoA carboxylic acid to form malonyl-CoA. The role of acetyl-CoA carboxylase 1 in fatty acid synthesis makes it a promising therapeutic target for various metabolic diseases such as non-alcoholic fatty liver disease, obesity and diabetes. Tumors have a high energy flow and a strong dependence on fatty acid synthesis. Thus, acetyl-CoA carboxylase inhibition has become a potential choice for anti-tumor therapy. In this review, we first introduced the structure and expression pattern of Acetyl-CoA carboxylase 1. We also discussed the molecular mechanisms of acetyl-CoA carboxylase 1 in the initiation and progression of various cancer types. Furthermore, acetyl-CoA carboxylase1 inhibitors has also been discussed. Collectively, we summarized the interplay between acetyl-CoA carboxylase 1 and tumorigenesis, indicating acetyl-CoA carboxylase 1 as a promising therapeutic target for tumor management.<\/jats:p>","DOI":"10.3389\/fphar.2023.1129010","type":"journal-article","created":{"date-parts":[[2023,2,10]],"date-time":"2023-02-10T04:33:57Z","timestamp":1676003637000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":31,"title":["Targeting acetyl-CoA carboxylase 1 for cancer therapy"],"prefix":"10.3389","volume":"14","author":[{"given":"Yong","family":"Yu","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qingzhu","family":"Nie","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ziyi","family":"Wang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yu","family":"Di","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaolong","family":"Chen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kaiming","family":"Ren","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2023,2,10]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"8180","DOI":"10.1158\/0008-5472.CAN-07-0389","article-title":"Chemical inhibition of acetyl-CoA carboxylase induces growth arrest and cytotoxicity selectively in cancer cells","volume":"67","author":"Beckers","year":"2007","journal-title":"Cancer Res."},{"key":"B2","doi-asserted-by":"publisher","first-page":"1363","DOI":"10.1016\/j.devcel.2021.04.013","article-title":"Lipid metabolism in cancer: New perspectives and emerging mechanisms","volume":"56","author":"Broadfield","year":"2021","journal-title":"Dev. 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