Fatty acid synthase and the lipogenic phenotype in cancer pathogenesis
Abstract
There is a renewed interest in the ultimate role of fatty acid synthase (FASN)--a key lipogenic enzyme catalysing the terminal steps in the de novo biogenesis of fatty acids--in cancer pathogenesis. Tumour-associated FASN, by conferring growth and survival advantages rather than functioning as an anabolic energy-storage pathway, appears to necessarily accompany the natural history of most human cancers. A recent identification of cross-talk between FASN and well-established cancer-controlling networks begins to delineate the oncogenic nature of FASN-driven lipogenesis. FASN, a nearly-universal druggable target in many human carcinomas and their precursor lesions, offers new therapeutic opportunities for metabolically treating and preventing cancer.
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FASN is highly expressed in colorectal cancer.
“We and others have previously reported that FASN is highly expressed in CRC [29,30].”
From Inhibition of fatty acid synthase enhances therapeutic efficacy and delays acquired resistance to BRAF-targeted therapy in colorectal cancer (2026) · cites this paper as [30]
FASN can promote cancer progression and contribute to therapy resistance by sustaining mitogenic signaling, facilitating the G1/S transition, and supplying lipid resources necessary for biomass accumulation and evasion of cell cycle checkpoints.
“FASN can promote cancer progression and contribute to therapy resistance by sustaining mitogenic signaling, facilitating the G1/S transition, and supplying lipid resources necessary for biomass accumulation and evasion of cell cycle checkpoints [30,48].”
From Inhibition of fatty acid synthase enhances therapeutic efficacy and delays acquired resistance to BRAF-targeted therapy in colorectal cancer (2026) · cites this paper as [30]
Cancer cells preferentially metabolize glucose by aerobic glycolysis, the Warburg effect.
“Cancer cells preferentially metabolize glucose by aerobic glycolysis, a phenomenon known as the Warburg effect.”
From An LXR Agonist Promotes Glioblastoma Cell Death through Inhibition of an EGFR/AKT/SREBP-1/LDLR–Dependent Pathway (2011) · cites this paper as [19]
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References 177 · Cited by 2,941
- Authors
- Menendez, J. A., & Lupu, R.
- Affiliations
- Northwestern University (US)
- Corresponding author
- Lupu, Ruth
- ORCID
- Lupu, Ruth
- Venue
- Nature Reviews Cancer
- Published
- 2007-10
- Volume
- 7
- Issue
- 10
- Pages
- 763-777
- ISSN
- 1474-175X (ISSN-L)
- 1474-1768
- OpenAlex
- W2153178365
- Cited by
- 2,941
- References
- 177
- Citations by year
- 2026: 118 · 2025: 159 · 2024: 257 · 2023: 177 · 2022: 217 · 2021: 222 · 2020: 200 · 2019: 184 · 2018: 166 · 2017: 162 · 2016: 199 · 2015: 172 · 2014: 171 · 2013: 142 · 2012: 118
- FWCI
- 5.34
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature reviews. Cancer (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Cancer Institute (R01CA116623)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Lipids, and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Lipid metabolism and biosynthesis
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Sphingolipid Metabolism and Signaling
- Keywords
- fatty acid synthase, lipogenesis, carcinogenesis, de novo lipogenesis, cancer metabolism, therapeutic target, metabolic therapy, cancer prevention
- MeSH terms
- Antineoplastic Agents, Carcinoma in Situ, Fatty Acids, Glucose, Humans, Multienzyme Complexes, Neoplasm Invasiveness, Neoplasm Metastasis, Neoplasms, Nuclear Proteins, Phenotype, Transcription Factors, Cell Death, Protein Serine-Threonine Kinases, Genes, BRCA1, Lipogenesis, Sterol Regulatory Element Binding Protein 1, AMP-Activated Protein Kinases, Fatty Acid Synthases
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