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. 2017 Jul 14;7:5384. doi: 10.1038/s41598-017-05541-4

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© The Author(s) 2017

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Schematic of the mechanism and magnificent background involved in this study. (A) Schematic of the insulin and PI3K/Akt signalling pathways. Dashed lines indicate a possible mechanism. (B) Schematic of the metabolic crosstalk between PC and skeletal muscle: ① UPS plays a key role in cancer patients’ experience of skeletal muscle loss; ② A close connection between the degree of severity of IR and progression of cancer cachexia; ③ IR exacerbates skeletal muscle degradation as cancer evolves, which produces amino acids for tumour proliferation; ④ Under the conditions of IR, overexpression of IRR and IGF-1 receptor in tumour cells promotes tumour growth.