Glucocorticoid receptor triggers a reversible drug-tolerant dormancy state with acquired therapeutic vulnerabilities in lung cancer

Glucocorticoid receptor triggers a reversible drug-tolerant dormancy state with acquired therapeutic vulnerabilities in lung cancer

Glucocorticoids (GC) are reported to block cancer cell proliferation, but the mode of action is unclear. Here the authors show that glucocorticoid receptor activation induces cancer cell dormancy in lung cancer by regulating CDKN1C expression through a distal enhancer, and these dormant cells are ad...

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Autores principales: Stefan Prekovic, Karianne Schuurman, Isabel Mayayo-Peralta, Anna G. Manjón, Mark Buijs, Selçuk Yavuz, Max D. Wellenstein, Alejandro Barrera, Kim Monkhorst, Anne Huber, Ben Morris, Cor Lieftink, Theofilos Chalkiadakis, Ferhat Alkan, Joana Silva, Balázs Győrffy, Liesbeth Hoekman, Bram van den Broek, Hans Teunissen, Donna O. Debets, Tesa Severson, Jos Jonkers, Timothy Reddy, Karin E. de Visser, William Faller, Roderick Beijersbergen, Maarten Altelaar, Elzo de Wit, Rene Medema, Wilbert Zwart
Formato: article
Lenguaje:EN
Publicado: Nature Portfolio 2021
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Science
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Acceso en línea:https://doaj.org/article/e4c712e9c2534821b3dbea828efb9470
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Sumario:Glucocorticoids (GC) are reported to block cancer cell proliferation, but the mode of action is unclear. Here the authors show that glucocorticoid receptor activation induces cancer cell dormancy in lung cancer by regulating CDKN1C expression through a distal enhancer, and these dormant cells are addicted to IGF-1R signalling pathway.

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