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Acetate Dependence of Tumors
Open accessAbstract
Acetyl-CoA represents a central node of carbon metabolism that plays a key role in bioenergetics, cell proliferation, and the regulation of gene expression. Highly glycolytic or hypoxic tumors must produce sufficient quantities of this metabolite to support cell growth and survival under nutrient-limiting conditions. Here, we show that the nucleocytosolic acetyl-CoA synthetase enzyme, ACSS2, supplies a key source of acetyl-CoA for tumors by capturing acetate as a carbon source. Despite exhibiting no gross deficits in growth or development, adult mice lacking ACSS2 exhibit a significant reduction in tumor burden in two different models of hepatocellular carcinoma. ACSS2 is expressed in a large proportion of human tumors, and its activity is responsible for the majority of cellular acetate uptake into both lipids and histones. These observations may qualify ACSS2 as a targetable metabolic vulnerability of a wide spectrum of tumors.
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“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 Comerford et al., 2014
In the citing paper
“Cancer cells are also able to generate acetyl-CoA from cytosolic acetate (Comerford et al., 2014; Gao et al., 2016; Kamphorst et al., 2014; Mashimo et al., 2014).”
From Targeting Metabolism for Cancer Therapy (2017) · cites this paper as Comerford et al., 2014
In the citing paper
“Some cancer types, including liver and glioblastomas, readily take up acetate, which can be converted to acetyl-CoA by ACSS and undergo oxidation in the TCA cycle (70, 195).”
From Regulation and function of the mammalian tricarboxylic acid cycle (2023) · cites this paper as [195]
In the citing paper
“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 Comerford et al., 2014
In the citing paper
“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 Comerford et al., 2014
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Cites
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Items 501–600 of 678
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InfluentialZhang, W., Yu, X., Lin, Y., Wu, C., Zhu, R., Jiang, X., Tao, J., Chen, Z., He, J., Zhang, X., et al. (2025) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-025-05689-7 · Cited by 5
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Histone modification as a reflection of metabolism
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“Acetyl-CoA is synthesized by Acetyl-CoA synthetase (AceCS2 in human and ACS in yeast) and by ATP-citrate lyase.(7) The levels of acetyl-CoA represent metabolic states.”
BackgroundMeynen, J., Adriaensens, P., Criel, M., Louis, E., Vanhove, K., Thomeer, M., Mesotten, L., & Derveaux, E. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25094690 · Cited by 5
“This was further confirmed by Comerford et al., who showed that ACSS2 knockdown in human patient tumor cell lines led to growth inhibition [48].”
ResultProteomic profiling reveals ACSS2 facilitating metabolic support in acute myeloid leukemia
Mochmann, L. H., Treue, D., Bockmayr, M. L., Silva, P., Zasada, C., Mastrobuoni, G., Bayram, Ş., Forbes, M., Jurmeister, P. S., Liebig, S., et al. (2024) · Cancer Gene Therapy · doi:10.1038/s41417-024-00785-5 · Cited by 6
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Conceptualizing Eukaryotic Metabolic Sensing and Signaling
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“Tumor cells can still save their situation because they have in the cytosol an enzyme, acetyl CoA synthetase directly converting incorporated acetate into acetyl CoA [17].”
BackgroundEpigenetic dysregulation in autophagy signaling as a driver of viral manifested oral carcinogenesis
Patra, S., Patil, S., Das, S., & Bhutia, S. K. (2022) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2022.166517 · Cited by 5
Leveraging insights into cancer metabolism—a symposium report
Cable, J., Finley, L. W. S., Tu, B. P., Patti, G. J., Oliver, T. G., Vardhana, S. A., Mana, M., Ericksen, R. E., Khare, S., DeBerardinis, R. J., et al. (2019) · Annals of the New York Academy of Sciences · doi:10.1111/nyas.14274 · Cited by 5
Self-citationCatabolic rewiring in cancer impacts dietary interventions
Chinopoulos, C. (2025) · Communications Biology · doi:10.1038/s42003-025-09333-9 · Cited by 6
“Acetyl-CoAsynthetase2isoften upregulatedincancer,activatingacetateintoacetyl-CoA,signi fi cantly contributing to lipid mediated-cell survival when other nutrients are limited 353 .”
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“We speculate the contradictory observations seen in our preclinical studies could be the result of the intrinsic property 11 C]-acetate PET rather than a fundamental difference in tumor metabolism in HCC [10, 28].”
BackgroundACSS2 gene variant associated with cleft lip and palate in two independent Hispanic populations
Dodhia, S., Celis, K., Aylward, A., Cai, Y., Fontana, M. E., Trespalacios, A., Hoffman, D. C., Alfonso, H. O., Eisig, S. B., Su, G. H., et al. (2017) · The Laryngoscope · doi:10.1002/lary.26637 · Cited by 4
“Specifically, among the three ACSS enzymes (ACSS1, ACSS2, and ACSS3), ACSS2 was found to have the greatest effect on acetate utilization in liver tumor cells, and mice with ACSS2 knockdowns had significantly lower tumor burdens than control mice.(23) Taken together, these studies all point to a role of ACSS2 in promot…”
BackgroundThe Impact of the Intestinal Microbiota in Therapeutic Responses Against Cancer
Bonvalet, M., Daillère, R., Roberti, M. P., Rauber, C., & Zitvogel, L. (2017) · Springer eBooks · doi:10.1007/978-3-319-62431-0_27 · Cited by 4
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Functional clusters analysis and research based on differential coexpression networks
Meng, S., Liu, G., Su, L., Sun, L., Wu, D., Wang, L., & Zheng, Z. S. (2017) · Biotechnology & Biotechnological Equipment · doi:10.1080/13102818.2017.1358669 · Cited by 4
“Some observations suggest ACSS2 to be expressed to a signi fi cant extent in particular tumour types, including triple-negtive breast cancers [30].”
BackgroundMetabolic Stress—Signaling and Metabolic Adaptation
Balakrishnan, P., Liebe, T., Amro, E. M., Dhaka, L., Heinzel, T., & Heller, R. (2018) · Elsevier eBooks · doi:10.1016/b978-0-12-814253-0.00012-7 · Cited by 5
Metabolic Reprogramming and Molecular Rewiring in Cancer: Therapeutic Opportunities
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Dialister in Microbiome of Cancer Patients: A Systematic Review and Meta-Analysis
Demırci, M. (2021) · Eurasian Journal of Medicine and Oncology · doi:10.14744/ejmo.2021.65073 · Cited by 4
“[13,14] Acetate has been reported as an important energy source for the development of solid tumors.[50] Similar to acetate, lactate has been reported as an important component of primary and metastatic cancer metabolism.”
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Expression of HIV-1 Reverse Transcriptase in Murine Cancer Cells Increases Mitochondrial Respiration
Zakirova, N. F., Kondrashova, A., Golikov, M. V., Ivanova, O. N., Ivanov, A. V., Isaguliants, M. G., & Олеговна, Б. Е. (2022) · Molecular Biology · doi:10.1134/s0026893322050168 · Cited by 4
“The uncoupling of glycolysis and the Krebs cycle does not mean a decrease in mitochondrial respiration since carbon donors can be generated by glutaminolysis [2], fatty acid oxidation [3], or direct conversion of acetyl coenzyme A from acetate [4, 5].”
Vignoli, A., Miolo, G., Tenori, L., Buonadonna, A., Lombardi, D., Steffan, A., Scalone, S., Luchinat, C., & Corona, G. (2023) · iScience · doi:10.1016/j.isci.2023.107678 · Cited by 4
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“Additionally, ACSS2 , ACADS , ACOX1 , and ACOX3 are essential in short-chain fatty acid metabolism, where ACSS2 catalyzes the formation of Crotonyl-CoA from crotonate, and ACADS , ACOX1 , and ACOX3 catalyze the conversion of butyryl-CoA to Crotonyl-CoA (19, 22, 23).”
Self-citationChen, H., Zeng, Y., Liu, L., Xu, W., Shi, Y., Ji, S., Xu, X., Yu, X., Hou, S., Qin, Y., et al. (2025) · Acta Biochimica et Biophysica Sinica · doi:10.3724/abbs.2025111 · Cited by 3
“Acetate (S8750, 1 mM) was purchased from Sigma - Aldrich (St Louis, USA) [19].”
Shi, K., Pan, B., Zheng, R., Liu, K., Song, J., Wang, X., & Li, L. (2025) · Frontiers in Immunology · doi:10.3389/fimmu.2025.1696102 · Cited by 4
“Depletion/reduction of ACSS2 has been reported to impair the growth of multiple cancer types, including breast, prostate, liver and glioblastomas (13 – 15).”
Abrams, R. P. M., Donahue, R., Ma, J., Mao, Y., Diolaiti, M. E., & Ashworth, A. (2025) · Cell Chemical Biology · doi:10.1016/j.chembiol.2025.10.006 · Cited by 2
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Self-citationACSS2 enables melanoma cell survival and tumor metastasis by negatively regulating the Hippo pathway
Zhang, B., Zhu, Q., Qu, D., Zhao, M., Du, J., Zhang, H., Wang, H., Jiang, L., Yi, X., Guo, S., et al. (2024) · Frontiers in Molecular Biosciences · doi:10.3389/fmolb.2024.1423795 · Cited by 3
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Basov, N. V., Adamovskaya, A. V., Rogachev, A. D., Gaisler, E. V., Сергеевич, Д. П., Ivanisenko, T., Сергеевич, В. А., Mishinov, S. V., Stupak, V. V., Cheresiz, S. V., et al. (2025) · Vavilov Journal of Genetics and Breeding · doi:10.18699/vjgb-24-96 · Cited by 3
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“Furthermore, we investigated whether the catalytic activity of ACSS2 is required for H3K9 acetylation by using a specific small-molecule ACSS2 inhibitor (ACSS2i) [23].”
Self-citationDesign, synthesis and photophysical studies of improved xanthene dye to detect acetate
Paredes, J. M., Miguel, D., Resa, S., González-García, M. C., Diaz-Torres, Y., Cuerva, J. M., & Crovetto, L. (2018) · Journal of Photochemistry and Photobiology A Chemistry · doi:10.1016/j.jphotochem.2018.11.032 · Cited by 3
“Based on it, we have synthesized a new Pennsylvania-based dye presenting an isopropyl group as substituent (Iso-PG) in order to obtain a pKa closer to acetate buffer and thus improve ESPT reaction, with the aim to be useful not only in the determination of acetate in human pathologies where its metabolism is involved,…”
MethodNutritional Influences on Epigenetics, Aging and Disease
Meiliana, A., Dewi, N. M., & Wijaya, A. (2019) · The Indonesian Biomedical Journal · doi:10.18585/inabj.v11i1.780 · Cited by 3
“Acetate then become an important carbon source for cancer cells, and is used to synthesize acetyl-CoA in challenging growth environments.(28,29) Another modification of histone that affect chromatin is methylation, where specific methylation marks can correlate with either active or repressed chromatin and this is als…”
BackgroundSCOT is a vital enzyme for tumors: With reference to Carney Triad Cancers and the ketogenic diet
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The potential effect and delivery of piperine on breast cancer
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Aspartate and Acetate Fuel Gastrointestinal Stromal Tumors Beyond the Warburg Effect
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“25,26 Acetyl-CoA, generated by the oxidation of glucose, glutamine, and acetate, is the central inter-mediary metabolite to biosynthesize nucleotides, amino acids, the cell membrane, and nuclear histone and transcription factor acetylation.”
Metabolic reprogramming and tumor immunity under hypoxic microenvironment
Yan, R., Sun, L., & Zhang, H. (2019) · Current Opinion in Physiology · doi:10.1016/j.cophys.2019.01.001 · Cited by 3
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“The cumulative effects of these compounds on the acetyl CoA formation in tumor cells might still be insufficient, since they develop a salvage pathway and they have in their cytosol an acetyl CoA synthetase capable of converting incorporated acetate into acetyl CoA, which then enters into the fatty acid synthesis and…”
BackgroundCancer RNome: Evolution and Sustenance
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Methionine coordinates a hierarchically organized anabolic program enabling proliferationPreprint
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ACSS2 regulates ferroptosis in an E2F1-dependent manner in breast cancer brain metastatic cellsPreprint
Esquea, E. M., Young, R. G., Ciraku, L., Merzy, J., Ahmed, N. N., Talarico, A. N., Karuppiah, M., Gocal, W. A., Simone, N. L., Dick, A., et al. (2024) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2024.10.18.619082 · Cited by 3
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“In a related publication, ACSS2 was found to be upregulated in glioblastoma compared to lower-grade lesions [34].”
Basappa, J., Goldman, A. R., Lobello, C., Wang, S., Rushmore, D., Melnikov, O., Sen, N. V., Mallikarjuna, V. S., Jain, P., Edalati, M., et al. (2026) · Cancer Letters · doi:10.1016/j.canlet.2026.218488 · Cited by 2
ACSS2 involved in acetyl‐ CoA synthesis regulates skeletal muscle function
Gunasekaran, M., Campos, G., Wells, N. M., Lambuu, K., Draper, I., Pacak, C. A., & Kang, P. B. (2025) · FEBS Letters · doi:10.1002/1873-3468.70152 · Cited by 2
“Our findings contrast with those of other studies that found no differences in the phenotype and litter size of Acss2 (cid:1) / (cid:1) mice [27,28].”
Oxidative stress and cancer metabolism: From pathogenesis to therapeutic opportunities
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From endoplasmic reticulum to nucleus: the fate of cellular fatty acids
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Metabolic pathway analysis of tumors using stable isotopes
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Highlights from the Literature
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“The implications for this are especially intriguing given recent evidence that mice deficient for ACSS2 have reduced tumor burden (Comerford et al., 2014).”
BackgroundThe DAXX-SREBP axis promotes oncogenic lipogenesis and tumorigenesisPreprint
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“DISCUSSION 21 ACSS2 has recognized functions in the dynamic interplay of stress responses, including 22 interaction with HIF-2α in the setting of adaptive responses to oxygen and nutrient limited states 23 [29, 30, 35, 36, 45].”
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“Similar tumor growth suppression was observed in triple-negative breast tumors with decreased ACSS2 expression 26 , as well as myeloma 27 and liver cancer 18 , where ACSS2 overexpression facilitated disease progression while inhibition decreased cell growth.”
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Metadata
- Authors
- Comerford, S. A., Huang, Z., Du, X., Wang, Y., Cai, L., Witkiewicz, A. K., Walters, H., Tantawy, M. N., Fu, A., Manning, H. C., Horton, J. D., Hammer, R. E., McKnight, S. L., & Tu, B. P.
- Affiliations
- The University of Texas Southwestern Medical Center (US)
- Vanderbilt University (US)
- Corresponding author
- McKnight, Steven L.
- Tu, Benjamin P.
- ORCID
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2014-12
- Volume
- 159
- Issue
- 7
- Pages
- 1591-1602
- ISSN
- 0092-8674 (ISSN-L)
- PMC
- PMC4272450
- OpenAlex
- W1972254548
- Cited by
- 681
- References
- 57
- Citations by year
- 2026: 32 · 2025: 55 · 2024: 71 · 2023: 68 · 2022: 61 · 2021: 67 · 2020: 52 · 2019: 55 · 2018: 57 · 2017: 59 · 2016: 63 · 2015: 38 · 2014: 3
- FWCI
- 17.35
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Damon Runyon Cancer Research Foundation
- University of Texas Southwestern Medical Center
- National Heart, Lung, and Blood Institute (P01HL020948)
- National Cancer Institute (P50CA095103, R01CA185169)
- 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
- ACSS2, acetyl-CoA synthetase, acetyl-CoA, acetate uptake, cancer metabolism, hepatocellular carcinoma, metabolic vulnerability, histone acetylation, tumor growth
- MeSH terms
- Acetates, Acetyl Coenzyme A, Acetate-CoA Ligase, Animals, Humans, Immunohistochemistry, Liver Neoplasms, Neoplasms, Positron-Emission Tomography, Mice, Triple Negative Breast Neoplasms
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