Formation of colorectal liver metastases induces musculoskeletal and metabolic abnormalities

Advanced colorectal cancer (CRC), a leading cause of death worldwide, is often accompanied by the development of liver metastases (LM), as well as skeletal muscle (SkM) wasting, i.e. cachexia. Despite affecting the majority of CRC patients, cachexia remains understudied and uncured. Moreover, only a single model of LM associated with CRC has been developed for the study of cachexia. Here we examined differential gene expression of skeletal muscles deriving from subcutaneous and metastatic C26 tumor hosts. Tumor hosts displaying LM experienced exacerbated muscle wasting compared to tumor hosts without LM. 8-week old CD2F1 male mice were subcutaneously (C26) or intrasplenically injected with C26 tumor cells (mC26) to mimic hepatic dissemination of cancer cells, while sham-operated animals received saline. All animals were euthanized weeks following experimental intervention. mRNA was isolated from quadriceps muscle. For RNA seq.