Metabolic Reprogramming in Cancer Cachexia

Cancer cachexia is a complex metabolic syndrome characterized by involuntary weight loss, skeletal muscle atrophy, adipose tissue remodeling, anorexia, and systemic inflammation. Affecting up to 80% of patients with advanced cancer, it is associated with poor prognosis and lacks effective therapies. This review focuses on metabolic reprogramming occurring between organs, integrating recent mechanistic insights into cross talk between central and peripheral tissues. Key mediators, including CCL2, IL-6, LIF, and GDF-15, are discussed in the context of neuroimmune and metabolic pathways that drive tissue wasting. Particular attention is given to the CCR2/CCL2 axis, which mediates immune cell infiltration into the brain, liver, and tumors, contributing to anorexia, muscle loss, and hepatic dysfunction. Understanding these integrated interorgan pathways highlights potential therapeutic targets to preserve metabolic homeostasis, improve functional outcomes, and extend survival in patients with cancer-associated cachexia.