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UCP2 induces metabolic reprogramming to inhibit proliferation of cancer cells

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

  • 1Inserm, 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.

Molecular & Cellular Oncology
|June 17, 2016
PubMed

Insights

Invalidating uncoupling protein 2 (Ucp2) boosts normal cell growth. Overexpressing Ucp2 in cancer cells reduces tumors by altering metabolism, suggesting Ucp2 combats tumorigenesis.

Area of Science:

  • Cellular metabolism
  • Cancer biology
  • Mitochondrial function

Background:

  • Uncoupling protein 2 (Ucp2) plays a role in cellular energy regulation.
  • Altered cellular metabolism, particularly increased glycolysis, is a hallmark of cancer.
  • The precise function of Ucp2 in cancer cell metabolism and tumorigenesis remains under investigation.

Purpose of the Study:

  • To investigate the role of Ucp2 in regulating cancer cell metabolism.
  • To determine the impact of Ucp2 expression levels on cancer cell proliferation and tumorigenicity.
  • To elucidate the metabolic switch associated with Ucp2 overexpression in cancer.

Main Methods:

  • Gene manipulation (invalidation and overexpression) of Ucp2 in normal and cancer cells.
  • Metabolic analysis, including glucose utilization and oxidative phosphorylation measurements.
  • Tumorigenicity assays in vivo and in vitro.

Main Results:

  • Invalidation of Ucp2 enhances glucose utilization and proliferation in normal cells.
  • Overexpression of Ucp2 in cancer cells leads to decreased tumorigenicity.
  • Ucp2-overexpressing cancer cells exhibit a metabolic shift from glycolysis to oxidative phosphorylation.

Conclusions:

  • Ucp2 is a critical regulator of cellular metabolism.
  • Ucp2 functions as a tumor suppressor by inhibiting tumorigenesis.
  • Targeting Ucp2 may offer a novel therapeutic strategy for cancer treatment.
Keywords:
cancermetabolism reprogrammingmitochondriaproliferationuncoupling protein 2

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