Drugging ACAT1 for Cancer Therapy

Javier Garcia-Bermudez; Kivanç Birsoy

doi:10.1016/j.molcel.2016.11.023

Drugging ACAT1 for Cancer Therapy

Mol Cell. 2016 Dec 1;64(5):856-857. doi: 10.1016/j.molcel.2016.11.023.

Authors

Javier Garcia-Bermudez¹, Kivanç Birsoy²

Affiliations

¹ Laboratory of Metabolic Regulation and Genetics, The Rockefeller University, 1230 York Avenue, New York, NY 10065, USA.
² Laboratory of Metabolic Regulation and Genetics, The Rockefeller University, 1230 York Avenue, New York, NY 10065, USA. Electronic address: [email protected].

PMID: 27912096
DOI: 10.1016/j.molcel.2016.11.023

Abstract

In this issue, Fan et al. (2016) show that oncogenic tyrosine kinases can promote glycolysis by phosphorylating and stabilizing the tetrameric form of mitochondrial acetyl-coA acetyltransferase 1 (ACAT1). The authors further identify a small molecule ACAT1 inhibitor that displays anti-cancer effects.

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MeSH terms

Acetyl-CoA C-Acetyltransferase*
Glycolysis
Humans
Mitochondria
Neoplasms
Protein-Tyrosine Kinases*

Substances

Acetyl-CoA C-Acetyltransferase
Protein-Tyrosine Kinases