Cancer-Associated Muscle Wasting-Candidate Mechanisms and Molecular Pathways

• Published in: International journal of molecular sciences Vol. 21; no. 23; p. 9268
• Main Authors: Armstrong, Victoria S, Fitzgerald, Liam W, Bathe, Oliver F
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 04.12.2020; MDPI
• Subjects: Apoptosis; Autophagy; Biomarkers; Cancer; Cancer therapies; Cytokines; Disease Susceptibility; Energy Metabolism; Humans; Inflammation; Inflammation Mediators - metabolism; Kinases; mediators; Muscle Development; muscle wasting; Muscle, Skeletal - metabolism; Muscle, Skeletal - pathology; Muscles; Musculoskeletal system; Neoplasms - complications; Pancreatic cancer; Pathogenesis; pathophysiology; Phagocytosis; Proteins; Proteolysis; Quality of life; Review; Sarcopenia; Sarcopenia - etiology; Sarcopenia - metabolism; Signal Transduction; Therapeutic applications; tumor; Tumor necrosis factor-TNF; Tumors; mediators; tumor; pathophysiology; tumor-derived; cancer; muscle wasting; sarcopenia
• ISSN: 1422-0067; 1661-6596; 1422-0067
• DOI: 10.3390/ijms21239268

Excessive muscle loss is commonly observed in cancer patients and its association with poor prognosis has been well-established. Cancer-associated sarcopenia differs from age-related wasting in that it is not responsive to nutritional intervention and exercise. This is related to its unique pathogenesis, a result of diverse and interconnected mechanisms including inflammation, disordered metabolism, proteolysis and autophagy. There is a growing body of evidence that suggests that the tumor is the driver of muscle wasting by its elaboration of mediators that influence each of these pro-sarcopenic pathways. In this review, evidence for these tumor-derived factors and putative mechanisms for inducing muscle wasting will be reviewed. Potential targets for future research and therapeutic interventions will also be reviewed.