Acetyl-CoA synthetase 2 promotes acetate utilization and maintains cancer cell growth under metabolic stress

Schug, Zachary T.; Peck, Barrie; Jones, Dylan T.; Zhang, Qifeng; Grosskurth, Shaun; Alam, Israt S.; Goodwin, Louise M.; Smethurst, Elizabeth; Mason, Susan; Blyth, Karen; McGarry, Lynn; James, Daniel; Shanks, Emma; Kalna, Gabriela; Saunders, Rebecca E.; Jiang, Ming; Howell, Michael; Lassailly, Francois; Thin, May Zaw; Spencer-Dene, Bradley; Stamp, Gordon; van den Broek, Niels J.F.; Mackay, Gillian; Bulusu, Vinay; Kamphorst, Jurre J.; Tardito, Saverio; Strachan, David; Harris, Adrian L.; Aboagye, Eric O.; Critchlow, Susan E.; Wakelam, Michael J.O.; Schulze, Almut; Gottlieb, Eyal

doi:10.1016/j.ccell.2014.12.002

Cited by 820Cancer, Lipids, and MetabolismCancer, Hypoxia, and MetabolismLipid metabolism and biosynthesis

Acetyl-CoA synthetase 2 promotes acetate utilization and maintains cancer cell growth under metabolic stress

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Schug, Zachary T., Peck, Barrie, Jones, Dylan T., Zhang, Qifeng, Grosskurth, Shaun, Alam, Israt S., Goodwin, Louise M., Smethurst, Elizabeth +25 more·2015·Cancer Cell

DOI 10.1016/j.ccell.2014.12.002PMC PMC4297291

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Abstract

A functional genomics study revealed that the activity of acetyl-CoA synthetase 2 (ACSS2) contributes to cancer cell growth under low-oxygen and lipid-depleted conditions. Comparative metabolomics and lipidomics demonstrated that acetate is used as a nutritional source by cancer cells in an ACSS2-dependent manner, and supplied a significant fraction of the carbon within the fatty acid and phospholipid pools. ACSS2 expression is upregulated under metabolically stressed conditions and ACSS2 silencing reduced the growth of tumor xenografts. ACSS2 exhibits copy-number gain in human breast tumors, and ACSS2 expression correlates with disease progression. These results signify a critical role for acetate consumption in the production of lipid biomass within the harsh tumor microenvironment.

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Some cancers depend on ACSS2 expression, making ACSS2 a potential therapeutic target.
“Some cancers are nevertheless dependent on expression of acetyl-CoA synthetase 2 (ACSS2), the cytosolic enzyme that allows cells to synthesize acetyl-CoA from acetate, making this represents a potential therapeutic target (Comerford et al., 2014; Schug et al., 2015).”
From Targeting Metabolism for Cancer Therapy (2017) · cites this paper as Schug et al., 2015
In cancer cells, citrate becomes labeled following supplementation with isotopically labeled acetate ([13C]acetate), indicating that acetate can undergo oxidation in the TCA cycle in cultured cell lines.
“In cancer cells, citrate becomes labeled following supplementation of cells with isotopically labeled acetate ([13C]acetate), indicating that acetate can undergo oxidation in the TCA cycle in cultured cell lines (69).”
From Regulation and function of the mammalian tricarboxylic acid cycle (2023) · cites this paper as [69]
Extracellular acetate is utilized by some cancers as source of acetyl-CoA for biosynthesis.
“Finally, extracellular acetate has recently been shown to be utilized by some cancers as a source of acetyl-CoA for biosynthesis.”
From The emerging hallmarks of cancer metabolism (2016) · cites this paper as Schug et al., 2015
Brain tumor types including primary glioblastomas and brain metastases assimilate exogenous acetate and incorporate acetate-derived carbons into de novo synthesized fatty acids.
“Specifically, a variety of tumor types localized to the brain, including primary glioblastomas as well as brain metastases that originated from other tissues, have been shown to assimilate exogenous acetate and incorporate acetate-derived carbons into de novo synthesized fatty acids (Comerford et al., 2014; Mashimo et al., 2014; Schug et al., 2015).”
From The emerging hallmarks of cancer metabolism (2016) · cites this paper as Schug et al., 2015

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(2000) · doi:10.1002/1097-0215(20001015)88:2

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“In cancer cells, citrate becomes labeled following supplementation of cells with isotopically labeled acetate ([(13)C] acetate), indicating that acetate can undergo oxidation in the TCA cycle in cultured cell lines (69).”
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Fatty acid synthesis is required for breast cancer brain metastasis
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Acetyl-coA synthetase 2 promotes acetate utilization and maintains cell growth under metabolic stress
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Authors: Schug, Z. T., Peck, B., Jones, D. T., Zhang, Q., Grosskurth, S., Alam, I. S., Goodwin, L. M., Smethurst, E., Mason, S., Blyth, K., McGarry, L., James, D., Shanks, E., Kalna, G., Saunders, R. E., Jiang, M., Howell, M., Lassailly, F., Thin, M. Z., Spencer-Dene, B., Stamp, G., van den Broek, N. J. F., Mackay, G., Bulusu, V., Kamphorst, J. J., Tardito, S., Strachan, D., Harris, A. L., Aboagye, E. O., Critchlow, S. E., Wakelam, M. J. O., Schulze, A., & Gottlieb, E.
Affiliations: Cancer Research UK Scotland Institute (GB)
Cancer Research UK (GB)
John Radcliffe Hospital (GB)
Babraham Institute (GB)
AstraZeneca (United Kingdom) (GB)
Hammersmith Hospital (GB)
University of Glasgow (GB)
Corresponding author: Gottlieb, Eyal
ORCID: Schug, Zachary T.
Peck, Barrie
Smethurst, Elizabeth
Mason, Susan
Blyth, Karen
McGarry, Lynn
James, Daniel
Shanks, Emma
Jiang, Ming
Howell, Michael
Thin, May Zaw
Stamp, Gordon
Mackay, Gillian
Bulusu, Vinay
Kamphorst, Jurre J.
Tardito, Saverio
Strachan, David
Harris, Adrian L.
Aboagye, Eric O.
Critchlow, Susan E.
Wakelam, Michael J.O.
Schulze, Almut
Gottlieb, Eyal
Venue: Cancer Cell
Publisher: Elsevier BV
Published: 2015-01
Volume: 27
Issue: 1
Pages: 57-71
ISSN: 1535-6108 (ISSN-L)
DOI: 10.1016/j.ccell.2014.12.002
PMC: PMC4297291
OpenAlex: W2044515618
Cited by: 820
References: 73
Citations by year: 2026: 64 · 2025: 76 · 2024: 96 · 2023: 72 · 2022: 88 · 2021: 75 · 2020: 63 · 2019: 67 · 2018: 68 · 2017: 57 · 2016: 63 · 2015: 28 · 2014: 1 · 2012: 1
FWCI: 23.79
Type: journal article
Language: en
Open access: hybrid
doi.org
Licence: cc-by-nc-nd
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
creativecommons.org/licenses/by-nc-nd/3.0/ (vor)
Locations: Cancer Cell (publishedVersion, cc-by-nc-nd)
PubMed Central (publishedVersion, cc-by-nc-nd)
PubMed (publishedVersion)
ENLIGHTEN (Jurnal Bimbingan dan Konseling Islam) (acceptedVersion)
Funders: AstraZeneca
Francis Crick Institute (10009, 10008)
Cancer Research UK (11359, 18278, 12011, 10337, 16466, 16584, 22311, 18974)
National Institute for Health and Care Research (NIHR/CS/009/009, NF-SI-0611-10163, EME/13/122/01)
Directorate for Biological Sciences
Medical Research Council (MR/J007986/1)
Biotechnology and Biological Sciences Research Council (BBS/E/B/000C0415, BBS/E/B/000C0413)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Lipids, and Metabolism
Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Lipid metabolism and biosynthesis
Keywords: acetyl-CoA synthetase 2, ACSS2, acetate utilization, cancer cell growth, metabolic stress, hypoxia, lipid depletion, tumor xenografts, fatty acid synthesis, phospholipid synthesis, tumor microenvironment, breast cancer, copy number gain, tumor progression
MeSH terms: Acetate-CoA Ligase, Animals, Hypoxia, Fatty Acids, Humans, Mice, Nude, Neoplasm Transplantation, Neoplasms, Stress, Physiological, Gene Expression Regulation, Neoplastic, Disease Progression, Gene Dosage, Cell Line, Tumor, Cell Proliferation, Mice, MCF-7 Cells

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Acetyl-CoA synthetase 2 promotes acetate utilization and maintains cancer cell growth under metabolic stress

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