Overcoming resistance to anabolic SARM therapy in experimental cancer cachexia with an HDAC inhibitor

Abstract No approved therapy exists for cancer‐associated cachexia. The colon‐26 mouse model of cancer cachexia mimics recent late‐stage clinical failures of anabolic anti‐cachexia therapy and was unresponsive to anabolic doses of diverse androgens, including the selective androgen receptor modulato...

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Main Authors: Sophia G Liva, Yu‐Chou Tseng, Anees M Dauki, Michael G Sovic, Trang Vu, Sally E Henderson, Yi‐Chiu Kuo, Jason A Benedict, Xiaoli Zhang, Bryan C Remaily, Samuel K Kulp, Moray Campbell, Tanios Bekaii‐Saab, Mitchell A Phelps, Ching‐Shih Chen, Christopher C Coss
Format: Article
Language:English
Published: Springer Nature 2020-01-01
Series:EMBO Molecular Medicine
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Online Access:https://doi.org/10.15252/emmm.201809910
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author Sophia G Liva
Yu‐Chou Tseng
Anees M Dauki
Michael G Sovic
Trang Vu
Sally E Henderson
Yi‐Chiu Kuo
Jason A Benedict
Xiaoli Zhang
Bryan C Remaily
Samuel K Kulp
Moray Campbell
Tanios Bekaii‐Saab
Mitchell A Phelps
Ching‐Shih Chen
Christopher C Coss
author_facet Sophia G Liva
Yu‐Chou Tseng
Anees M Dauki
Michael G Sovic
Trang Vu
Sally E Henderson
Yi‐Chiu Kuo
Jason A Benedict
Xiaoli Zhang
Bryan C Remaily
Samuel K Kulp
Moray Campbell
Tanios Bekaii‐Saab
Mitchell A Phelps
Ching‐Shih Chen
Christopher C Coss
author_sort Sophia G Liva
collection DOAJ
description Abstract No approved therapy exists for cancer‐associated cachexia. The colon‐26 mouse model of cancer cachexia mimics recent late‐stage clinical failures of anabolic anti‐cachexia therapy and was unresponsive to anabolic doses of diverse androgens, including the selective androgen receptor modulator (SARM) GTx‐024. The histone deacetylase inhibitor (HDACi) AR‐42 exhibited anti‐cachectic activity in this model. We explored combined SARM/AR‐42 therapy as an improved anti‐cachectic treatment paradigm. A reduced dose of AR‐42 provided limited anti‐cachectic benefits, but, in combination with GTx‐024, significantly improved body weight, hindlimb muscle mass, and grip strength versus controls. AR‐42 suppressed the IL‐6/GP130/STAT3 signaling axis in muscle without impacting circulating cytokines. GTx‐024‐mediated β‐catenin target gene regulation was apparent in cachectic mice only when combined with AR‐42. Our data suggest cachectic signaling in this model involves catabolic signaling insensitive to anabolic GTx‐024 therapy and a blockade of GTx‐024‐mediated anabolic signaling. AR‐42 mitigates catabolic gene activation and restores anabolic responsiveness to GTx‐024. Combining GTx‐024, a clinically established anabolic therapy, with AR‐42, a clinically evaluated HDACi, represents a promising approach to improve anabolic response in cachectic patients.
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spelling doaj-art-e590447d2f534e9b86dfa986d39f3eb82025-08-20T03:43:21ZengSpringer NatureEMBO Molecular Medicine1757-46761757-46842020-01-0112212110.15252/emmm.201809910Overcoming resistance to anabolic SARM therapy in experimental cancer cachexia with an HDAC inhibitorSophia G Liva0Yu‐Chou Tseng1Anees M Dauki2Michael G Sovic3Trang Vu4Sally E Henderson5Yi‐Chiu Kuo6Jason A Benedict7Xiaoli Zhang8Bryan C Remaily9Samuel K Kulp10Moray Campbell11Tanios Bekaii‐Saab12Mitchell A Phelps13Ching‐Shih Chen14Christopher C Coss15Division of Pharmaceutics and Pharmacology, College of Pharmacy, The Ohio State UniversityDivision of Medicinal Chemistry and Pharmacognosy, College of Pharmacy, The Ohio State UniversityDivision of Pharmaceutics and Pharmacology, College of Pharmacy, The Ohio State UniversityDivision of Pharmaceutics and Pharmacology, College of Pharmacy, The Ohio State UniversityDivision of Pharmaceutics and Pharmacology, College of Pharmacy, The Ohio State UniversityDepartment of Veterinary Biosciences, College of Veterinary Medicine, Ohio State UniversityDivision of Medicinal Chemistry and Pharmacognosy, College of Pharmacy, The Ohio State UniversityCenter for Biostatistics, Department of Biomedical Informatics, The Ohio State UniversityCenter for Biostatistics, Department of Biomedical Informatics, The Ohio State UniversityDivision of Pharmaceutics and Pharmacology, College of Pharmacy, The Ohio State UniversityDivision of Pharmaceutics and Pharmacology, College of Pharmacy, The Ohio State UniversityDivision of Pharmaceutics and Pharmacology, College of Pharmacy, The Ohio State UniversityMayo Clinic Cancer CenterDivision of Pharmaceutics and Pharmacology, College of Pharmacy, The Ohio State UniversityDivision of Medicinal Chemistry and Pharmacognosy, College of Pharmacy, The Ohio State UniversityDivision of Pharmaceutics and Pharmacology, College of Pharmacy, The Ohio State UniversityAbstract No approved therapy exists for cancer‐associated cachexia. The colon‐26 mouse model of cancer cachexia mimics recent late‐stage clinical failures of anabolic anti‐cachexia therapy and was unresponsive to anabolic doses of diverse androgens, including the selective androgen receptor modulator (SARM) GTx‐024. The histone deacetylase inhibitor (HDACi) AR‐42 exhibited anti‐cachectic activity in this model. We explored combined SARM/AR‐42 therapy as an improved anti‐cachectic treatment paradigm. A reduced dose of AR‐42 provided limited anti‐cachectic benefits, but, in combination with GTx‐024, significantly improved body weight, hindlimb muscle mass, and grip strength versus controls. AR‐42 suppressed the IL‐6/GP130/STAT3 signaling axis in muscle without impacting circulating cytokines. GTx‐024‐mediated β‐catenin target gene regulation was apparent in cachectic mice only when combined with AR‐42. Our data suggest cachectic signaling in this model involves catabolic signaling insensitive to anabolic GTx‐024 therapy and a blockade of GTx‐024‐mediated anabolic signaling. AR‐42 mitigates catabolic gene activation and restores anabolic responsiveness to GTx‐024. Combining GTx‐024, a clinically established anabolic therapy, with AR‐42, a clinically evaluated HDACi, represents a promising approach to improve anabolic response in cachectic patients.https://doi.org/10.15252/emmm.201809910androgencachexiaHDAC inhibitorselective androgen receptor modulatorSTAT3
spellingShingle Sophia G Liva
Yu‐Chou Tseng
Anees M Dauki
Michael G Sovic
Trang Vu
Sally E Henderson
Yi‐Chiu Kuo
Jason A Benedict
Xiaoli Zhang
Bryan C Remaily
Samuel K Kulp
Moray Campbell
Tanios Bekaii‐Saab
Mitchell A Phelps
Ching‐Shih Chen
Christopher C Coss
Overcoming resistance to anabolic SARM therapy in experimental cancer cachexia with an HDAC inhibitor
EMBO Molecular Medicine
androgen
cachexia
HDAC inhibitor
selective androgen receptor modulator
STAT3
title Overcoming resistance to anabolic SARM therapy in experimental cancer cachexia with an HDAC inhibitor
title_full Overcoming resistance to anabolic SARM therapy in experimental cancer cachexia with an HDAC inhibitor
title_fullStr Overcoming resistance to anabolic SARM therapy in experimental cancer cachexia with an HDAC inhibitor
title_full_unstemmed Overcoming resistance to anabolic SARM therapy in experimental cancer cachexia with an HDAC inhibitor
title_short Overcoming resistance to anabolic SARM therapy in experimental cancer cachexia with an HDAC inhibitor
title_sort overcoming resistance to anabolic sarm therapy in experimental cancer cachexia with an hdac inhibitor
topic androgen
cachexia
HDAC inhibitor
selective androgen receptor modulator
STAT3
url https://doi.org/10.15252/emmm.201809910
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