ATP citrate lyase is an important component of cell growth and transformation
Abstract
Cell proliferation requires a constant supply of lipids and lipid precursors to fuel membrane biogenesis and protein modification. Cytokine stimulation of hematopoietic cells directly stimulates glucose utilization in excess of bioenergetic demand, resulting in a shift from oxidative to glycolytic metabolism. A potential benefit of this form of metabolism is the channeling of glucose into biosynthetic pathways. Here we report that glucose supports de novo lipid synthesis in growing hematopoietic cells in a manner regulated by cytokine availability and the PI 3 K/Akt signaling pathway. The net conversion of glucose to lipid is dependent on the ability of cells to produce cytosolic acetyl CoA from mitochondria-derived citrate through the action of ATP citrate lyase (ACL). Stable knockdown of ACL leads to a significant impairment of glucose-dependent lipid synthesis and an elevation of mitochondrial membrane potential. Cells with ACL knockdown display decreased cytokine-stimulated cell proliferation. In contrast, these cells resist cell death induced by either cytokine or glucose withdrawal. However, ACL knockdown significantly impairs Akt-mediated tumorigenesis in vivo. These data suggest that enzymes involved in the conversion of glucose to lipid may be targets for the treatment of pathologic cell growth.
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Targeting ACLY genetically or chemically prevents xenograft tumor formation and proliferation.
“ACLY activity is elevated in cancers (Migita et al., 2008), and targeting ACLY genetically or chemically prevents xenograft tumor formation and proliferation (Adam et al., 2013; Bauer et al., 2005; Hatzivassiliou et al., 2005; Migita et al., 2008).”
From Targeting Metabolism for Cancer Therapy (2017) · cites this paper as Bauer et al., 2005
Akt activates ACLY, which cleaves TCA-derived citrate into acetyl-CoA and oxaloacetate.
“To this end, Akt activates the ATP-citrate lyase (ACLY) enzyme, which catalyzes cytosol-localized cleavage of the TCA cycle-derived citrate into acetyl-CoA and oxaloacetate (Bauer et al., 2005; Berwick et al., 2002).”
From The emerging hallmarks of cancer metabolism (2016) · cites this paper as Bauer et al., 2005
PI3K/Akt activation allows a cell to expand its cytosolic acetyl-CoA pool, a substrate for de novo fatty acid biosynthesis.
“In particular, PI3K/Akt activation allows a cell to expand its cytosolic pool of acetyl-CoA, a substrate for the de novo biosynthesis of fatty acids.”
From The emerging hallmarks of cancer metabolism (2016) · cites this paper as Bauer et al., 2005
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- Authors
- Bauer, D. E., Hatzivassiliou, G., Zhao, F., Andreadis, C., & Thompson, C. B.
- Affiliations
- Abramson Cancer Center (US)
- University of Pennsylvania (US)
- Corresponding author
- Thompson, Craig B
- Venue
- Oncogene
- Published
- 2005-06-13
- Volume
- 24
- Issue
- 41
- Pages
- 6314-6322
- ISSN
- 0950-9232 (ISSN-L)
- 1476-5594
- OpenAlex
- W2064318855
- Cited by
- 537
- References
- 46
- Citations by year
- 2026: 10 · 2025: 17 · 2024: 22 · 2023: 26 · 2022: 38 · 2021: 37 · 2020: 29 · 2019: 31 · 2018: 23 · 2017: 26 · 2016: 36 · 2015: 41 · 2014: 37 · 2013: 27 · 2012: 37
- FWCI
- 3.92
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Oncogene (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Damon Runyon Cancer Research Foundation
- 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 › PI3K/AKT/mTOR signaling in cancer
- Keywords
- ATP citrate lyase, de novo lipogenesis, hematopoietic cells, cytokine induction, PI3K/Akt signaling, mitochondrial membrane potential, cell proliferation, cell transformation, carcinogenesis, glucose deprivation, cell death resistance, metabolic reprogramming
- MeSH terms
- Amino Acid Sequence, ATP Citrate (pro-S)-Lyase, Cell Division, Cell Line, Cell Transformation, Neoplastic, Flow Cytometry, Molecular Sequence Data
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