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

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 meta...

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Autores principales:	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
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Neoplasms. Tumors. Oncology. Including cancer and carcinogens RC254-282
Acceso en línea:	https://doaj.org/article/3ffbeeb5d8f0457d99bab6179b071ed7
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spelling	oai:doaj.org-article:3ffbeeb5d8f0457d99bab6179b071ed72021-12-02T16:19:32ZMetabolic reprogramming underlies metastatic potential in an obesity-responsive murine model of metastatic triple negative breast cancer10.1038/s41523-017-0027-52374-4677https://doaj.org/article/3ffbeeb5d8f0457d99bab6179b071ed72017-07-01T00:00:00Zhttps://doi.org/10.1038/s41523-017-0027-5https://doaj.org/toc/2374-4677Triple 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.Ciara H. O’FlanaganEmily L. RossiShannon B. McDonellXuewen ChenYi-Hsuan TsaiJoel S. ParkerJerry UsaryCharles M. PerouStephen D. HurstingNature PortfolioarticleNeoplasms. Tumors. Oncology. Including cancer and carcinogensRC254-282ENnpj Breast Cancer, Vol 3, Iss 1, Pp 1-11 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Neoplasms. Tumors. Oncology. Including cancer and carcinogens RC254-282
spellingShingle	Neoplasms. Tumors. Oncology. Including cancer and carcinogens RC254-282 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 Metabolic reprogramming underlies metastatic potential in an obesity-responsive murine model of metastatic triple negative breast cancer
description	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.
format	article
author	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
author_facet	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
author_sort	Ciara H. O’Flanagan
title	Metabolic reprogramming underlies metastatic potential in an obesity-responsive murine model of metastatic triple negative breast cancer
title_short	Metabolic reprogramming underlies metastatic potential in an obesity-responsive murine model of metastatic triple negative breast cancer
title_full	Metabolic reprogramming underlies metastatic potential in an obesity-responsive murine model of metastatic triple negative breast cancer
title_fullStr	Metabolic reprogramming underlies metastatic potential in an obesity-responsive murine model of metastatic triple negative breast cancer
title_full_unstemmed	Metabolic reprogramming underlies metastatic potential in an obesity-responsive murine model of metastatic triple negative breast cancer
title_sort	metabolic reprogramming underlies metastatic potential in an obesity-responsive murine model of metastatic triple negative breast cancer
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/3ffbeeb5d8f0457d99bab6179b071ed7
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Metabolic reprogramming underlies metastatic potential in an obesity-responsive murine model of metastatic triple negative breast cancer

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