Statins Limit Coenzyme Q Synthesis and Metabolically Synergize with MEK Inhibition in Pancreatic Tumors.
basic_science · Level V
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- Record sourced from PubMed, PMID 31941676.
- Also identified by DOI 10.1158/0008-5472.CAN-19-3415.
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Abstract
Tumors frequently increase expression of enzymes in the mevalonate biosynthesis pathway. Statins inhibit flux through this pathway, but if and how such treatments elicit a therapeutic benefit in cancer remains unclear. In this issue of <i>Cancer Research</i>, McGregor and colleagues perform <i>in vivo</i> metabolic tracing to demonstrate that mouse pancreatic ductal adenocarcinoma (PDAC) tumors and human PDAC cell lines require this pathway for coenzyme Q (CoQ) synthesis and redox homeostasis. Simvastatin treatment reduces CoQ synthesis and promotes oxidative stress and apoptosis in tumors when administered in combination with a MEK inhibitor, providing a new mechanism through which statin treatment may impact PDAC growth.<i>See related article by McGregor et al., p. 175</i>.
Medical subject headings
- Carcinoma, Pancreatic Ductal
- Hydroxymethylglutaryl-CoA Reductase Inhibitors
- Pancreatic Neoplasms