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

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Ataxin-10 is part of a cachexokine cocktail triggering cardiac metabolic dysfunction in cancer cachexia. / Schäfer, Michaela; Oeing, Christian U; Rohm, Maria; Baysal-Temel, Ezgi; Lehmann, Lorenz H; Bauer, Ralf; Volz, H Christian; Boutros, Michael; Sohn, Daniela; Sticht, Carsten; Gretz, Norbert; Eichelbaum, Katrin; Werner, Tessa; Hirt, Marc N; Eschenhagen, Thomas; Müller-Decker, Karin; Strobel, Oliver; Hackert, Thilo; Krijgsveld, Jeroen; Katus, Hugo A; Berriel Diaz, Mauricio; Backs, Johannes; Herzig, Stephan.

In: MOL METAB, Vol. 5, No. 2, 02.2016, p. 67-78.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Schäfer, M, Oeing, CU, Rohm, M, Baysal-Temel, E, Lehmann, LH, Bauer, R, Volz, HC, Boutros, M, Sohn, D, Sticht, C, Gretz, N, Eichelbaum, K, Werner, T, Hirt, MN, Eschenhagen, T, Müller-Decker, K, Strobel, O, Hackert, T, Krijgsveld, J, Katus, HA, Berriel Diaz, M, Backs, J & Herzig, S 2016, 'Ataxin-10 is part of a cachexokine cocktail triggering cardiac metabolic dysfunction in cancer cachexia', MOL METAB, vol. 5, no. 2, pp. 67-78. https://doi.org/10.1016/j.molmet.2015.11.004

APA

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., ... Herzig, S. (2016). Ataxin-10 is part of a cachexokine cocktail triggering cardiac metabolic dysfunction in cancer cachexia. MOL METAB, 5(2), 67-78. https://doi.org/10.1016/j.molmet.2015.11.004

Vancouver

Schäfer M, Oeing CU, Rohm M, Baysal-Temel E, Lehmann LH, Bauer R et al. Ataxin-10 is part of a cachexokine cocktail triggering cardiac metabolic dysfunction in cancer cachexia. MOL METAB. 2016 Feb;5(2):67-78. https://doi.org/10.1016/j.molmet.2015.11.004

Bibtex

@article{b1d604599b3e4d15bb7d9a30f100924c,
title = "Ataxin-10 is part of a cachexokine cocktail triggering cardiac metabolic dysfunction in cancer cachexia",
abstract = "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.",
keywords = "Journal Article",
author = "Michaela Sch{\"a}fer and Oeing, {Christian U} and Maria Rohm and Ezgi Baysal-Temel and Lehmann, {Lorenz H} and Ralf Bauer and Volz, {H Christian} and Michael Boutros and Daniela Sohn and Carsten Sticht and Norbert Gretz and Katrin Eichelbaum and Tessa Werner and Hirt, {Marc N} and Thomas Eschenhagen and Karin M{\"u}ller-Decker and Oliver Strobel and Thilo Hackert and Jeroen Krijgsveld and Katus, {Hugo A} and {Berriel Diaz}, Mauricio and Johannes Backs and Stephan Herzig",
year = "2016",
month = feb,
doi = "10.1016/j.molmet.2015.11.004",
language = "English",
volume = "5",
pages = "67--78",
journal = "MOL METAB",
issn = "2212-8778",
publisher = "Elsevier GmbH",
number = "2",

}

RIS

TY - JOUR

T1 - Ataxin-10 is part of a cachexokine cocktail triggering cardiac metabolic dysfunction in cancer cachexia

AU - Schäfer, Michaela

AU - Oeing, Christian U

AU - Rohm, Maria

AU - Baysal-Temel, Ezgi

AU - Lehmann, Lorenz H

AU - Bauer, Ralf

AU - Volz, H Christian

AU - Boutros, Michael

AU - Sohn, Daniela

AU - Sticht, Carsten

AU - Gretz, Norbert

AU - Eichelbaum, Katrin

AU - Werner, Tessa

AU - Hirt, Marc N

AU - Eschenhagen, Thomas

AU - Müller-Decker, Karin

AU - Strobel, Oliver

AU - Hackert, Thilo

AU - Krijgsveld, Jeroen

AU - Katus, Hugo A

AU - Berriel Diaz, Mauricio

AU - Backs, Johannes

AU - Herzig, Stephan

PY - 2016/2

Y1 - 2016/2

N2 - 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.

AB - 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.

KW - Journal Article

U2 - 10.1016/j.molmet.2015.11.004

DO - 10.1016/j.molmet.2015.11.004

M3 - SCORING: Journal article

C2 - 26909315

VL - 5

SP - 67

EP - 78

JO - MOL METAB

JF - MOL METAB

SN - 2212-8778

IS - 2

ER -