UCP2 induces metabolic reprogramming to inhibit proliferation of cancer cells

Pauline Esteves; Claire Pecqueur; Marie-Clotilde Alves-Guerra

doi:10.4161/23723556.2014.975024

UCP2 induces metabolic reprogramming to inhibit proliferation of cancer cells

Mol Cell Oncol. 2014 Dec 1;2(1):e975024. doi: 10.4161/23723556.2014.975024. eCollection 2015 Jan-Mar.

Authors

Pauline Esteves¹, Claire Pecqueur², Marie-Clotilde Alves-Guerra³

Affiliations

¹ Inserm, U1016; Institut Cochin; Paris, 75014, France; CNRS; UMR 8104; Paris, France; Université Paris Descartes; Sorbonne Paris Cité; Paris, France; These authors contributed equally to this article.
² CRCNA - UMR 892 INSERM - 6299 CNRS; Nantes, France; Faculté de Médecine; Université de Nantes; Nantes, France; These authors contributed equally to this article.
³ Inserm, U1016; Institut Cochin; Paris, 75014, France; CNRS; UMR 8104; Paris, France; Université Paris Descartes; Sorbonne Paris Cité; Paris, France.

Abstract

Invalidation of uncoupling protein 2 (Ucp2) increases glucose utilization and proliferation in normal cells. We recently reported that cancer cells that overexpress UCP2 become less tumorigenic while switching their metabolism from glycolysis to oxidative phosphorylation. UCP2 appears to be a key regulator of cellular metabolism with a relevant function against tumorigenesis.

Keywords: cancer; metabolism reprogramming; mitochondria; proliferation; uncoupling protein 2.