| Literature DB >> 29920276 |
Parash Parajuli1, Santosh Kumar1, Audrey Loumaye2, Purba Singh1, Sailaja Eragamreddy1, Thien Ly Nguyen1, Seval Ozkan1, Mohammed S Razzaque3, Céline Prunier4, Jean-Paul Thissen2, Azeddine Atfi5.
Abstract
Cancer cachexia is characterized by extreme skeletal muscle loss that results in high morbidity and mortality. The incidence of cachexia varies among tumor types, being lowest in sarcomas, whereas 90% of pancreatic ductal adenocarcinoma (PDAC) patients experience severe weight loss. How these tumors trigger muscle depletion is still unfolding. Serendipitously, we found that overexpression of Twist1 in mouse muscle progenitor cells, either constitutively during development or inducibly in adult animals, caused severe muscle atrophy with features reminiscent of cachexia. Using several genetic mouse models of PDAC, we detected a marked increase in Twist1 expression in muscle undergoing cachexia. In cancer patients, elevated levels of Twist1 are associated with greater degrees of muscle wasting. Finally, both genetic and pharmacological inactivation of Twist1 in muscle progenitor cells afforded substantial protection against cancer-mediated cachexia, which translated into meaningful survival benefits, implicating Twist1 as a possible target for attenuating muscle cachexia in cancer patients.Entities:
Keywords: Activin/Myostatin cytokines; Smad signaling; Twist1; cancer cachexia; muscle cachexia; muscle progenitor cells; muscle protein breakdown; pancreatic ductal adenocarcinoma
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Year: 2018 PMID: 29920276 PMCID: PMC6054474 DOI: 10.1016/j.devcel.2018.05.026
Source DB: PubMed Journal: Dev Cell ISSN: 1534-5807 Impact factor: 12.270