FIGURE 6.

Schematic representation of the effect of NYT on the melanoma-induced cancer cachexia in mice. Details are provided in the text. In brief, phosphorylation of AMP kinase in cancer cachexia mouse skeletal muscle is caused by the increase of inflammatory cytokines, tumor-necrosis factor-α, free fatty acids which is released from adipocytes. Moreover, these changes might be decreased the phosphorylation of 4E-BP1 in skeletal muscle of mice with cancer cachexia. NYT normalizes the increased phosphorylation of AMP kinase and the decreased phosphorylation of 4E-BP1 through the functional changes of adipocyte and inhibition of STAT3 signaling. The action site of NYT indicated as cross mark. Bold lines indicate enhancement in cancer cachexia model. Pale colored lines indicate the reduced signaling in cancer cachexia.