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A molecular pathway for cancer cachexia-induced muscle atrophy revealed at single-nucleus resolution.
Zhang, Yichi; Dos Santos, Matthieu; Huang, Huocong; Chen, Kenian; Iyengar, Puneeth; Infante, Rodney; Polanco, Patricio M; Brekken, Rolf A; Cai, Chunyu; Caijgas, Ambar; Cano Hernandez, Karla; Xu, Lin; Bassel-Duby, Rhonda; Liu, Ning; Olson, Eric N.
Afiliación
  • Zhang Y; Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA; Hamon Center for Regenerative Science and Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
  • Dos Santos M; Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA; Hamon Center for Regenerative Science and Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
  • Huang H; Department of Surgery, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA; Hamon Center for Therapeutic Oncology Research, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
  • Chen K; Quantitative Biomedical Research Center, Peter O'Donnell Jr. School of Public Health, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
  • Iyengar P; Department of Radiation Oncology, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA.
  • Infante R; Center for Human Nutrition, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
  • Polanco PM; Department of Surgery, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
  • Brekken RA; Department of Surgery, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA; Hamon Center for Therapeutic Oncology Research, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
  • Cai C; Department of Pathology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
  • Caijgas A; Department of Neuroscience, UT Southwestern Medical Center, Dallas, TX 75390, USA.
  • Cano Hernandez K; Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA; Hamon Center for Regenerative Science and Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
  • Xu L; Quantitative Biomedical Research Center, Peter O'Donnell Jr. School of Public Health, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
  • Bassel-Duby R; Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA; Hamon Center for Regenerative Science and Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
  • Liu N; Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA; Hamon Center for Regenerative Science and Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. Electronic address: ning.liu@utsouthwestern.edu.
  • Olson EN; Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA; Hamon Center for Regenerative Science and Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. Electronic address: eric.olson@utsouthwestern.edu.
Cell Rep ; 43(8): 114587, 2024 Aug 27.
Article en En | MEDLINE | ID: mdl-39116208
ABSTRACT
Cancer cachexia is a prevalent and often fatal wasting condition that cannot be fully reversed with nutritional interventions. Muscle atrophy is a central component of the syndrome, but the mechanisms whereby cancer leads to skeletal muscle atrophy are not well understood. We performed single-nucleus multi-omics on skeletal muscles from a mouse model of cancer cachexia and profiled the molecular changes in cachexic muscle. Our results revealed the activation of a denervation-dependent gene program that upregulates the transcription factor myogenin. Further studies showed that a myogenin-myostatin pathway promotes muscle atrophy in response to cancer cachexia. Short hairpin RNA inhibition of myogenin or inhibition of myostatin through overexpression of its endogenous inhibitor follistatin prevented cancer cachexia-induced muscle atrophy in mice. Our findings uncover a molecular basis of muscle atrophy associated with cancer cachexia and highlight potential therapeutic targets for this disorder.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Caquexia / Atrofia Muscular / Miogenina / Miostatina Límite: Animals / Humans / Male Idioma: En Revista: Cell Rep Año: 2024 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Estados Unidos
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Caquexia / Atrofia Muscular / Miogenina / Miostatina Límite: Animals / Humans / Male Idioma: En Revista: Cell Rep Año: 2024 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Estados Unidos