ATP citrate lyase inhibition can suppress tumor cell growth.

By G. Hatzivassiliou, F. Zhao, Daniel E. Bauer, C. Andreadis, A. Shaw, D. Dhanak, S. Hingorani, D. Tuveson, Craig B. Thompson. Cancer Cell, 2005

1,018 citations recorded by the source corpus.

Subfields: Cancer Research, Oncology

View Paper: https://www.semanticscholar.org/paper/b27c41822a157b67f6dedbb656111097c4588256

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cancer Research

1. M. V. Vander Heiden
2. C. V. Dang
3. Ralph J. Deberardinis
4. David M. Sabatini
5. Craig B. Thompson
6. G. Semenza
7. Sophia Y. Lunt
8. Guido Kroemer

In Oncology

1. Guido Kroemer
2. M. V. Vander Heiden
3. L. Galluzzi
4. Ralph J. Deberardinis
5. David M. Sabatini
6. Craig B. Thompson
7. Russell G. Jones
8. M. C. Simon

Citations in the corpus

• Lipid metabolism reprogramming and its potential targets in cancer (2018, background): “The ACLY inhibitor SB-204990 strongly inhibits tumor growth in mice with lung, prostate or ovarian cancer xenografts [162, 165].”
• Aerobic glycolysis: meeting the metabolic requirements of cell proliferation. (2011, positive): “The ability to generate cytosolic acetyl-coA is critical for cell proliferation (Hatzivassiliou et al 2005).”
• Fueling Immunity: Insights into Metabolism and Lymphocyte Function (2013, methodology): “In this model, mitochondrial citrate is formed from condensation of oxaloacetate and acetyl-CoA, after which citrate is exported from the mitochondrion to the cytosol and converted back to acetyl-CoA by ATP citrate lyase (ACL) (47).”
• Acetyl-CoA Synthetase 2 Promotes Acetate Utilization and Maintains Cancer Cell Growth under Metabolic Stress (2015, background): “It has been shown that ACLY is required for cell growth and cancer cell survival, and there has been interest in the development of ACLY inhibitors, with some showing potential at inhibiting tumor growth (Beckers et al., 2007; Hatzivassiliou et al., 2005; Zu et al., 2012).”
• Fatty acid synthase and the lipogenic phenotype in cancer pathogenesis (2007, background): “Markedly increased ACLY expression and activity have been reported in cancer cell”
• Memory CD8+ T cells use cell intrinsic lipolysis to support the metabolic programming necessary for development (2014, background): “Alternatively, IL-15 memory T cells might be able to switch from using ACL derived acetyl-CoA to that produced from acetate via acylCoA synthetase, an effect previously observed after ACL deletion (Hatzivassiliou et al., 2005; Zaidi et al., 2012).”
• Hooked on fat: the role of lipid synthesis in cancer metabolism and tumour development (2013, background): “Moreover, silencing of ACLY has been shown to block cancer cell growth both in vivo and in vitro (Bauer et al., 2005; Hatzivassiliou et al., 2005).”
• Targeting metabolic transformation for cancer therapy (2010, background): “SB-204990 has been shown to inhibit ACLY ( Table 1 ), and was also reported to limit both tumour cell proliferation and survival in vitro”
• Cancer cell metabolism: Warburg and beyond. (2008, background): “Inhibition of ATP citrate lyase, the distal enzyme that converts mitochondrial-derived citrate into cytosolic acetyl coenzyme A, the precursor for many lipid species, prevents cancer cell proliferation and tumor growth (Hatzivassiliou et al., 2005).”
• Metabolic Reprogramming: A Cancer Hallmark Even Warburg Did Not Anticipate (2012, background): “Akt facilitates this diversion of mitochondrial citrate from the TCA cycle to acetyl-CoA production by phosphorylating and activating ACL (Bauer et al., 2005; Berwick et al., 2002; Hatzivassiliou et al., 2005).”