npj Breast Cancer (Jul 2017)

Metabolic reprogramming underlies metastatic potential in an obesity-responsive murine model of metastatic triple negative breast cancer

  • Ciara H. O’Flanagan,
  • Emily L. Rossi,
  • Shannon B. McDonell,
  • Xuewen Chen,
  • Yi-Hsuan Tsai,
  • Joel S. Parker,
  • Jerry Usary,
  • Charles M. Perou,
  • Stephen D. Hursting

DOI
https://doi.org/10.1038/s41523-017-0027-5
Journal volume & issue
Vol. 3, no. 1
pp. 1 – 11

Abstract

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Triple negative breast cancer: Obesity and metabolism fuel disease spread Metabolic changes contribute to the metastatic potential of triple negative breast cancer (TNBC), a mouse study shows. Stephen Hursting and colleagues from the University of North Carolina at Chapel Hill, USA, established metastatic mouse TNBC cells driven by Wnt-1, a signaling protein that’s highly active in this aggressive subtype of breast cancer. In a lab dish, these cells showed signs of increased invasiveness; and when transplanted into mice, the cells readily formed tumors that metastasized to the lungs. Obese mice experienced more aggressive tumor growth and spread than normal-weight animals. Gene expression analyses revealed that TNBC cells with metastatic potential have an energetic leg-up over their non-metastatic counterparts in the face of obesity-induced metabolic changes, suggesting that targeting metabolic perturbations could help reduce the burden of metastatic TNBC, particularly for obese women.