Cachexia is a severe condition characterized by significant weight loss due to the depletion of skeletal muscle and adipose tissue, primarily affecting patients with advanced cancer. This review aims to provide an overview of the molecular mechanisms underlying cachexia and potential therapeutic targets. Cachexia is associated with poor prognosis, increased surgical complications, chemotherapy toxicity, functional impairments, and fatigue. Early detection of cancer cachexia can improve quality of life and survival rates, but current biomarkers have limitations and are not universally applicable. The molecular mechanisms of cachexia involve an imbalance between anabolic and catabolic processes, with factors such as decreased anabolic hormone levels, amino acid loss, and muscle inactivity contributing to muscle atrophy. Inflammation, driven by cytokines like TNF-α and IL-6, plays a crucial role in muscle wasting by inducing proteolysis and disrupting the anabolic-catabolic balance. The TGF-β superfamily proteins, including myostatin and activin, are potent inhibitors of muscle growth and are elevated in cachectic conditions. The IGF-1/PI3K/AKT pathway, which regulates muscle growth, is inhibited by myostatin and activin. Non-coding RNAs, such as miRNAs, also play a significant role in gene expression regulation and may serve as potential biomarkers and therapeutic targets. Additionally, signaling pathways like JNK, SIRT1-NOX4, and Toll-like receptor/MyD88/XBP1 are involved in the development of cachexia. Targeting these pathways and molecules could potentially mitigate muscle atrophy and improve outcomes in cancer cachexia.Cachexia is a severe condition characterized by significant weight loss due to the depletion of skeletal muscle and adipose tissue, primarily affecting patients with advanced cancer. This review aims to provide an overview of the molecular mechanisms underlying cachexia and potential therapeutic targets. Cachexia is associated with poor prognosis, increased surgical complications, chemotherapy toxicity, functional impairments, and fatigue. Early detection of cancer cachexia can improve quality of life and survival rates, but current biomarkers have limitations and are not universally applicable. The molecular mechanisms of cachexia involve an imbalance between anabolic and catabolic processes, with factors such as decreased anabolic hormone levels, amino acid loss, and muscle inactivity contributing to muscle atrophy. Inflammation, driven by cytokines like TNF-α and IL-6, plays a crucial role in muscle wasting by inducing proteolysis and disrupting the anabolic-catabolic balance. The TGF-β superfamily proteins, including myostatin and activin, are potent inhibitors of muscle growth and are elevated in cachectic conditions. The IGF-1/PI3K/AKT pathway, which regulates muscle growth, is inhibited by myostatin and activin. Non-coding RNAs, such as miRNAs, also play a significant role in gene expression regulation and may serve as potential biomarkers and therapeutic targets. Additionally, signaling pathways like JNK, SIRT1-NOX4, and Toll-like receptor/MyD88/XBP1 are involved in the development of cachexia. Targeting these pathways and molecules could potentially mitigate muscle atrophy and improve outcomes in cancer cachexia.