Wang Hang, Li Tsung-Lin, Hsia Simon, Su I-Li, Chan Yi-Lin, Wu Chang-Jer
Department of Food Science, National Taiwan Ocean University, Keelung, Taiwan.
Institute of Biomedical Nutrition, Hung Kuang University, Taichung, Taiwan.
Oncotarget. 2015 Apr 10;6(10):7758-73. doi: 10.18632/oncotarget.3483.
Chemotherapy can cause cachexia, which is manifested by weight loss, inflammation and muscle atrophy. However, the mechanisms of tumor and chemotherapy on skeletal muscle proteolysis, remained unclear. In this report, we demonstrated that tumor-induced myostatin in turn induced TNF-α, thus activating calcium-dependent and proteasomal protein degradation. Chemotherapy activated myostatin-mediated proteolysis and muscle atrophy by elevating IL-6. In tumor-bearing mice under chemotherapy, supplementation with fish oil and selenium prevented a rise in IL-6, TNF-α and myostatin and muscle atrophy. The findings presented here allow us to better understand the molecular basis of cancer cachexia and potentiate nutrition supplementation in future cancer chemotherapy.
化疗可导致恶病质，表现为体重减轻、炎症和肌肉萎缩。然而，肿瘤和化疗对骨骼肌蛋白水解的机制仍不清楚。在本报告中，我们证明肿瘤诱导的肌肉生长抑制素反过来诱导肿瘤坏死因子-α，从而激活钙依赖性和蛋白酶体蛋白降解。化疗通过升高白细胞介素-6激活肌肉生长抑制素介导的蛋白水解和肌肉萎缩。在化疗的荷瘤小鼠中，补充鱼油和硒可防止白细胞介素-6、肿瘤坏死因子-α和肌肉生长抑制素升高以及肌肉萎缩。此处呈现的研究结果使我们能够更好地理解癌症恶病质的分子基础，并在未来的癌症化疗中加强营养补充。
