Gain Fat-Lose Metastasis: Converting Invasive Breast Cancer Cells into Adipocytes Inhibits Cancer Metastasis.

Autor:	Ishay-Ronen D; Department of Biomedicine, University of Basel, Mattenstrasse 28, 4058 Basel, Switzerland. Electronic address: pandanaro@gmail.com., Diepenbruck M; Department of Biomedicine, University of Basel, Mattenstrasse 28, 4058 Basel, Switzerland., Kalathur RKR; Department of Biomedicine, University of Basel, Mattenstrasse 28, 4058 Basel, Switzerland., Sugiyama N; Department of Biomedicine, University of Basel, Mattenstrasse 28, 4058 Basel, Switzerland., Tiede S; Department of Biomedicine, University of Basel, Mattenstrasse 28, 4058 Basel, Switzerland., Ivanek R; Department of Biomedicine, University of Basel, Mattenstrasse 28, 4058 Basel, Switzerland., Bantug G; University Hospital Basel, Department of Biomedicine, University of Basel, Switzerland., Morini MF; Department of Biomedicine, University of Basel, Mattenstrasse 28, 4058 Basel, Switzerland., Wang J; Department of Biomedicine, University of Basel, Mattenstrasse 28, 4058 Basel, Switzerland., Hess C; University Hospital Basel, Department of Biomedicine, University of Basel, Switzerland., Christofori G; Department of Biomedicine, University of Basel, Mattenstrasse 28, 4058 Basel, Switzerland. Electronic address: gerhard.christofori@unibas.ch.
Jazyk:	angličtina
Zdroj:	Cancer cell [Cancer Cell] 2019 Jan 14; Vol. 35 (1), pp. 17-32.e6.
DOI:	10.1016/j.ccell.2018.12.002
Abstrakt:	Cancer cell plasticity facilitates the development of therapy resistance and malignant progression. De-differentiation processes, such as an epithelial-mesenchymal transition (EMT), are known to enhance cellular plasticity. Here, we demonstrate that cancer cell plasticity can be exploited therapeutically by forcing the trans-differentiation of EMT-derived breast cancer cells into post-mitotic and functional adipocytes. Delineation of the molecular pathways underlying such trans-differentiation has motivated a combination therapy with MEK inhibitors and the anti-diabetic drug Rosiglitazone in various mouse models of murine and human breast cancer in vivo. This combination therapy provokes the conversion of invasive and disseminating cancer cells into post-mitotic adipocytes leading to the repression of primary tumor invasion and metastasis formation. (Copyright © 2018 Elsevier Inc. All rights reserved.)
Databáze:	MEDLINE
Externí odkaz:	Zobrazit plný text záznamu