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Effects of CRF2R agonist on tumor growth and cachexia in mice implanted with Lewis lung carcinoma cells
Author(s) -
Argilés Josep M.,
Figueras Maite,
Ametller Elisabet,
Fuster Gemma,
Olivan Mireia,
de Oliveira Cibely Cristine Fontes,
LópezSoriano Francisco J.,
Isfort Robert J.,
Busquets Sílvia
Publication year - 2008
Publication title -
muscle and nerve
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.025
H-Index - 145
eISSN - 1097-4598
pISSN - 0148-639X
DOI - 10.1002/mus.20899
Subject(s) - cachexia , lewis lung carcinoma , agonist , wasting , skeletal muscle , endocrinology , medicine , gastrocnemius muscle , lung cancer , cancer , receptor , biology , metastasis
Previous studies have demonstrated an effect of corticotropin‐releasing factor 2 receptor (CRF2R) agonists in the maintenance of skeletal muscle mass. The aim of this study was to evaluate the effects of a CRF2R agonist in preserving skeletal muscle in a mouse cachexia model. Implantation of a fast‐growing tumor to mice (Lewis lung carcinoma) resulted in a clear cachectic state characterized by a profound muscle wasting. We found that administration of a CRF2R agonist (PG‐873637) at 100 μg/kg/day by means of osmotic minipumps to tumor‐bearing mice resulted in beneficial effects on muscle weight loss. Thus, muscle loss was partially reversed by the CRF2R agonist at different stages of tumor growth (at day 14 after tumor inoculation: 12% in tibialis posterior; 9% in gastrocnemius; and 48% in soleus). Moreover, the CRF2R agonist significantly reduced both the number of metastases and their mass (at day 19 after tumor inoculation: 66% and 61%, respectively). These data suggest a potentially beneficial effect of the CRF2R agonist in preserving skeletal muscle during cancer cachexia and open a line of research for the development of new therapeutic approaches for the treatment of muscle wasting associated with cancer. Muscle Nerve, 2007