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Despite being responsible for one third of all cancer deaths, cachexia is generally under\u2010studied in OC due to a limited number of pre\u2010clinical animal models. We aimed to address this gap by characterizing the cachectic phenotype in a mouse model of OC.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Nod SCID gamma mice (<jats:italic>n<\/jats:italic> = 6\u201310) were injected intraperitoneally with 1 \u00d7 10<jats:sup>7<\/jats:sup> ES\u20102 human OC cells to mimic disseminated abdominal disease. Muscle size and strength, as well as bone morphometry, were assessed. Tumour\u2010derived effects on muscle fibres were investigated in C2C12 myotube cultures. IL\u20106 levels were detected in serum and ascites from tumour hosts, as well as in tumour sections.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>In about 2 weeks, ES\u20102 cells developed abdominal tumours infiltrating omentum, mesentery, and adjacent organs. The ES\u20102 tumours caused severe cachexia with marked loss of body weight (\u201312%, <jats:italic>P<\/jats:italic> &lt; 0.01) and ascites accumulation in the peritoneal cavity (4.7 \u00b1 1.5 mL). Skeletal muscles appeared markedly smaller in the tumour\u2010bearing mice (approximately \u201335%, <jats:italic>P<\/jats:italic> &lt; 0.001). Muscle loss was accompanied by fibre atrophy, consistent with reduced muscle cross\u2010sectional area (\u201334%, <jats:italic>P<\/jats:italic> &lt; 0.01) and muscle weakness (\u201350%, <jats:italic>P<\/jats:italic> &lt; 0.001). Body composition assessment by dual\u2010energy X\u2010ray absorptiometry revealed decreased bone mineral density (\u20138%, <jats:italic>P<\/jats:italic> &lt; 0.01) and bone mineral content (\u201319%, <jats:italic>P<\/jats:italic> &lt; 0.01), also consistent with reduced trabecular bone in both femurs and vertebrae, as suggested by micro\u2010CT imaging of bone morphometry. In the ES\u20102 mouse model, cachexia was also associated with high tumour\u2010derived IL\u20106 levels in plasma and ascites (26.3 and 279.6 pg\/mL, respectively) and with elevated phospho\u2010STAT3 (+274%, <jats:italic>P<\/jats:italic> &lt; 0.001), reduced phospho\u2010AKT (\u201344%, <jats:italic>P<\/jats:italic> &lt; 0.001) and decreased mitochondrial proteins, as well as with increased protein ubiquitination (+42%, <jats:italic>P<\/jats:italic> &lt; 0.001) and expression of ubiquitin ligases in the skeletal muscle of tumour hosts. Similarly, ES\u20102 conditioned medium directly induced fibre atrophy in C2C12 mouse myotubes (\u201316%, <jats:italic>P<\/jats:italic> &lt; 0.001), consistent with elevated phospho\u2010STAT3 (+1.4\u2010fold, <jats:italic>P<\/jats:italic> &lt; 0.001) and altered mitochondrial homoeostasis and metabolism, while inhibition of the IL\u20106\/STAT3 signalling by means of INCB018424 was sufficient to restore the myotubes size.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>Our results suggest that the development of ES\u20102 OC promotes muscle atrophy in both <jats:italic>in vivo<\/jats:italic> and <jats:italic>in vitro<\/jats:italic> conditions, accompanied by loss of bone mass, enhanced muscle protein catabolism, abnormal mitochondrial homoeostasis, and elevated IL\u20106 levels. Therefore, this represents an appropriate model for the study of OC cachexia. Our model will aid in identifying molecular mediators that could be effectively targeted in order to improve muscle wasting associated with OC.<\/jats:p><\/jats:sec>","DOI":"10.1002\/jcsm.12311","type":"journal-article","created":{"date-parts":[[2018,7,16]],"date-time":"2018-07-16T04:15:01Z","timestamp":1531714501000},"page":"685-700","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":90,"title":["Growth of ovarian cancer xenografts causes loss of muscle and bone mass: a new model for the study of cancer cachexia"],"prefix":"10.1002","volume":"9","author":[{"given":"Fabrizio","family":"Pin","sequence":"first","affiliation":[{"name":"Department of Anatomy and Cell Biology Indiana University School of Medicine  Indianapolis IN 46202 USA"},{"name":"Indiana Center for Musculoskeletal Health Indiana University School of Medicine  Indianapolis IN 46202 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