American Association for Cancer Research
00085472can133383-sup-123287_1_supp_0_n9xlm0.pdf (88.95 kB)

Data Supplement from Mitochondrial Retrograde Signaling Mediated by UCP2 Inhibits Cancer Cell Proliferation and Tumorigenesis

Download (88.95 kB)
journal contribution
posted on 2023-03-30, 22:30 authored by Pauline Esteves, Claire Pecqueur, Céline Ransy, Catherine Esnous, Véronique Lenoir, Frédéric Bouillaud, Anne-Laure Bulteau, Anne Lombès, Carina Prip-Buus, Daniel Ricquier, Marie-Clotilde Alves-Guerra

Table S1. UCP2 mRNA levels in different cancers (Oncomine data)



Cancer cells tilt their energy production away from oxidative phosphorylation (OXPHOS) toward glycolysis during malignant progression, even when aerobic metabolism is available. Reversing this phenomenon, known as the Warburg effect, may offer a generalized anticancer strategy. In this study, we show that overexpression of the mitochondrial membrane transport protein UCP2 in cancer cells is sufficient to restore a balance toward oxidative phosphorylation and to repress malignant phenotypes. Altered expression of glycolytic and oxidative enzymes mediated the effects of this metabolic shift. Notably, UCP2 overexpression increased signaling from the master energy-regulating kinase, adenosine monophosphate-activated protein kinase, while downregulating expression of hypoxia-induced factor. In support of recent new evidence about UCP2 function, we found that UCP2 did not function in this setting as a membrane potential uncoupling protein, but instead acted to control routing of mitochondria substrates. Taken together, our results define a strategy to reorient mitochondrial function in cancer cells toward OXPHOS that restricts their malignant phenotype. Cancer Res; 74(14); 3971–82. ©2014 AACR.

Usage metrics

    Cancer Research



    Ref. manager