Cancer cachexia is a complex metabolic syndrome characterized by significant weight loss, skeletal muscle atrophy, and fat loss, often associated with advanced cancer. This review summarizes the molecular mechanisms underlying cachexia and potential therapeutic targets. Cachexia is driven by an imbalance between anabolic and catabolic processes, with factors such as inflammation, cytokines, and metabolic changes contributing to muscle and fat loss. Key mediators include transforming growth factor-beta (TGF-β), tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and myostatin, which promote muscle atrophy and fat loss. The molecular pathways involved include the mTOR, JNK, and SIRT1-NOX4 signaling pathways, as well as the role of non-coding RNAs and Toll-like receptors (TLRs). The review also highlights the role of inflammatory cytokines in cachexia and the potential of targeting these pathways for therapeutic intervention. Despite the complexity of the condition, current treatments are limited, and further research is needed to develop effective therapies. Biomarkers such as GDF-15, activin A, and miRNAs are being explored for early detection and monitoring of cachexia. The review emphasizes the importance of understanding the molecular mechanisms of cachexia to develop targeted therapies that can improve patient outcomes.Cancer cachexia is a complex metabolic syndrome characterized by significant weight loss, skeletal muscle atrophy, and fat loss, often associated with advanced cancer. This review summarizes the molecular mechanisms underlying cachexia and potential therapeutic targets. Cachexia is driven by an imbalance between anabolic and catabolic processes, with factors such as inflammation, cytokines, and metabolic changes contributing to muscle and fat loss. Key mediators include transforming growth factor-beta (TGF-β), tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and myostatin, which promote muscle atrophy and fat loss. The molecular pathways involved include the mTOR, JNK, and SIRT1-NOX4 signaling pathways, as well as the role of non-coding RNAs and Toll-like receptors (TLRs). The review also highlights the role of inflammatory cytokines in cachexia and the potential of targeting these pathways for therapeutic intervention. Despite the complexity of the condition, current treatments are limited, and further research is needed to develop effective therapies. Biomarkers such as GDF-15, activin A, and miRNAs are being explored for early detection and monitoring of cachexia. The review emphasizes the importance of understanding the molecular mechanisms of cachexia to develop targeted therapies that can improve patient outcomes.