Research Papers:

Skeletal muscle atrophy is attenuated in tumor-bearing mice under chemotherapy by treatment with fish oil and selenium

Hang Wang, Tsung-Lin Li, Simon Hsia, I-Li Su, Yi-Lin Chan and Chang-Jer Wu _

PDF  |  HTML  |  Supplementary Files  |  How to cite

Oncotarget. 2015; 6:7758-7773. https://doi.org/10.18632/oncotarget.3483

Metrics: PDF 3510 views  |   HTML 2813 views  |   ?  


Hang Wang1,3, Tsung-Lin Li2, Simon Hsia3, I-Li Su4, Yi-Lin Chan5 and Chang-Jer Wu1,6

1 Department of Food Science, National Taiwan Ocean University, Keelung, Taiwan

2 Genomics Research Center, Academia Sinica, Taipei, Taiwan

3 Institute of Biomedical Nutrition, Hung Kuang University, Taichung, Taiwan

4 Antai Medical Care Cooperation Antai Tian-Sheng Memorial Hospital, Pingtung, Taiwan

5 Department of Life Science, Chinese Culture University, Taipei, Taiwan

6 Center of Excellence for the Oceans, National Taiwan Ocean University, Keelung, Taiwan

Correspondence to:

Chang-Jer Wu, email:

Yi-Lin Chan, email:

Keywords: muscle atrophy, cachexia, fish oil, selenium, chemotherapy

Received: November 19, 2014 Accepted: February 04, 2015 Published: March 07, 2015


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.

Creative Commons License All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 4.0 License.
PII: 3483