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Nuclear lamin A/C phosphorylation by loss of androgen receptor leads to cancer-associated fibroblast activation.
Ghosh, Soumitra; Isma, Jovan; Ostano, Paola; Mazzeo, Luigi; Toniolo, Annagiada; Das, Monalisa; White, Joni R; Simon, Christian; Paolo Dotto, G.
Afiliación
  • Ghosh S; Personalised Cancer Prevention Unit, ORL Service, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland. soumitra.ghosh@pilani.bits-pilani.ac.in.
  • Isma J; Department of Immunobiology, University of Lausanne, Epalinges, Switzerland. soumitra.ghosh@pilani.bits-pilani.ac.in.
  • Ostano P; Department of Biological Sciences, Birla Institute of Technology and Science (BITS) Pilani Campus, Pilani, India. soumitra.ghosh@pilani.bits-pilani.ac.in.
  • Mazzeo L; Department of Immunobiology, University of Lausanne, Epalinges, Switzerland.
  • Toniolo A; Cutaneous Biology Research Center, Department of Dermatology, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, USA.
  • Das M; Cancer Genomics Laboratory, Edo and Elvo Tempia Valenta Foundation, Biella, Italy.
  • White JR; Department of Immunobiology, University of Lausanne, Epalinges, Switzerland.
  • Simon C; Department of Immunobiology, University of Lausanne, Epalinges, Switzerland.
  • Paolo Dotto G; Department of Immunobiology, University of Lausanne, Epalinges, Switzerland.
Nat Commun ; 15(1): 7984, 2024 Sep 12.
Article en En | MEDLINE | ID: mdl-39266569
ABSTRACT
Alterations in nuclear structure and function are hallmarks of cancer cells. Little is known about these changes in Cancer-Associated Fibroblasts (CAFs), crucial components of the tumor microenvironment. Loss of the androgen receptor (AR) in human dermal fibroblasts (HDFs), which triggers early steps of CAF activation, leads to nuclear membrane changes and micronuclei formation, independent of cellular senescence. Similar changes occur in established CAFs and are reversed by restoring AR activity. AR associates with nuclear lamin A/C, and its loss causes lamin A/C nucleoplasmic redistribution. AR serves as a bridge between lamin A/C and the protein phosphatase PPP1. Loss of AR decreases lamin-PPP1 association and increases lamin A/C phosphorylation at Ser 301, a characteristic of CAFs. Phosphorylated lamin A/C at Ser 301 binds to the regulatory region of CAF effector genes of the myofibroblast subtype. Expression of a lamin A/C Ser301 phosphomimetic mutant alone can transform normal fibroblasts into tumor-promoting CAFs.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Receptores Androgénicos / Núcleo Celular / Lamina Tipo A / Fibroblastos Asociados al Cáncer Límite: Humans / Male Idioma: En Revista: Nat Commun Asunto de la revista: BIOLOGIA / CIENCIA Año: 2024 Tipo del documento: Article País de afiliación: Suiza Pais de publicación: Reino Unido
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Receptores Androgénicos / Núcleo Celular / Lamina Tipo A / Fibroblastos Asociados al Cáncer Límite: Humans / Male Idioma: En Revista: Nat Commun Asunto de la revista: BIOLOGIA / CIENCIA Año: 2024 Tipo del documento: Article País de afiliación: Suiza Pais de publicación: Reino Unido