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Schäfer, M. ; Oeing, C.U.* ; Rohm, M. ; Baysal-Temel, E.* ; Lehmann, L.H.* ; Bauer, R.* ; Volz, H.C.* ; Boutros, M.* ; Sohn, D.* ; Sticht, C.* ; Gretz, N.* ; Eichelbaum, K.* ; Werner, T.* ; Hirt, M.N.* ; Eschenhagen, T.* ; Müller-Decker, K.* ; Strobel, O.* ; Hackert, T.* ; Krijgsveld, J.* ; Katus, H.A.* ; Berriel Diaz, M. ; Backs, J.* ; Herzig, S.

Ataxin-10 is part of a cachexokine cocktail triggering cardiac metabolic dysfunction in cancer cachexia.

Mol. Metab. 5, 67-78 (2016)

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Objectives Cancer cachexia affects the majority of tumor patients and significantly contributes to high mortality rates in these subjects. Despite its clinical importance, the identity of tumor-borne signals and their impact on specific peripheral organ systems, particularly the heart, remain mostly unknown. Methods and Results By combining differential colon cancer cell secretome profiling with large-scale cardiomyocyte phenotyping, we identified a signature panel of seven “cachexokines”, including Bridging integrator 1, Syntaxin 7, Multiple inositol-polyphosphate phosphatase 1, Glucosidase alpha acid, Chemokine ligand 2, Adamts like 4, and Ataxin-10, which were both sufficient and necessary to trigger cardiac atrophy and aberrant fatty acid metabolism in cardiomyocytes. As a prototypical example, engineered secretion of Ataxin-10 from non-cachexia-inducing cells was sufficient to induce cachexia phenotypes in cardiomyocytes, correlating with elevated Ataxin-10 serum levels in murine and human cancer cachexia models. Conclusions As Ataxin-10 serum levels were also found to be elevated in human cachectic cancer patients, the identification of Ataxin-10 as part of a cachexokine cocktail now provides a rational approach towards personalized predictive, diagnostic and therapeutic measures in cancer cachexia.

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