Oncostatin M signaling drives cancer-associated skeletal muscle wasting

Investigating muscle wasting in a murine model of cancer cachexia, we identified Oncostatin M (OSM) as a potential mediator of inflammatory responses in skeletal muscle. OSM is a member of the IL-6 family of cytokines and has crucial functions in cell growth, differentiation, and inflammation. Our results demonstrate that OSM induces muscle atrophy. To understand if its effect is specific or it is a general effect of IL6 family cytokines, primary myotubes were treated with OSM, IL6 and LIF for 48hrs. Our findings showed that OSM potently induces muscle wasting in differentiated myotubes. Overall design: Primary myoblasts were differentiated to myotubes and treated with recombinant OSM, IL-6 and LIF for 48hrs. The RNA was isolated and sent for sequencing.