Cancer cachexia is a syndrome characterized by a marked weight loss, anorexia, asthenia and anemia. The degree of cachexia is inversely correlated with the survival time of the patient and it always implies a poor prognosis. Lean body mass depletion is one of the main trends of cachexia and it involves not only skeletal muscle but it also affects cardiac protein. The main aim of the present review is to summarize and evaluate the different molecular mechanisms and catabolic mediators (both humoural and tumoural) involved in cancer cachexia since they may represent targets for future promising clinical investigations.