Amelioration of muscle wasting by gintonin in cancer cachexia

Cancer cachexia is characterized by systemic inflammation, protein degradation, and loss of skeletal muscle. Despite extensive efforts to develop therapeutics, only few effective treatments are available to protect against cancer cachexia. Here, we found that gintonin (GT), a ginseng-derived lysopho...

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Autores principales:	Yoseph Toni Wijaya, Tania Setiawan, Ita Novita Sari, Seung-Yeol Nah, Hyog Young Kwon
Formato:	article
Lenguaje:	EN
Publicado:	Elsevier 2021
Materias:	Gintonin Muscle atrophy Cancer cachexia Oxidative stress Neoplasms. Tumors. Oncology. Including cancer and carcinogens RC254-282
Acceso en línea:	https://doaj.org/article/91368fd2de874bc5b0c3fd49f3a1625e
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id	oai:doaj.org-article:91368fd2de874bc5b0c3fd49f3a1625e
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spelling	oai:doaj.org-article:91368fd2de874bc5b0c3fd49f3a1625e2021-11-30T04:14:42ZAmelioration of muscle wasting by gintonin in cancer cachexia1476-558610.1016/j.neo.2021.11.008https://doaj.org/article/91368fd2de874bc5b0c3fd49f3a1625e2021-12-01T00:00:00Zhttp://www.sciencedirect.com/science/article/pii/S1476558621000981https://doaj.org/toc/1476-5586Cancer cachexia is characterized by systemic inflammation, protein degradation, and loss of skeletal muscle. Despite extensive efforts to develop therapeutics, only few effective treatments are available to protect against cancer cachexia. Here, we found that gintonin (GT), a ginseng-derived lysophosphatidic acid receptor (LPAR) ligand, protected C2C12 myotubes from tumor necrosis factor α (TNFα)/interferon γ (IFNγ)- induced muscle wasting condition. The activity of GT was found to be dependent on LPAR/Gαi2, as the LPAR antagonist Ki16425 and Gαi2 siRNA abolished the anti-atrophic effects of GT on myotubes. GT suppressed TNFα-induced oxidative stress by reducing reactive oxygen species and suppressing inflammation-related genes, such as interleukin 6 (IL-6) and NADPH oxidase 2 (NOX-2). In addition, GT exhibited anti-atrophy effects in primary normal human skeletal myoblasts. Further, GT protected against Lewis lung carcinoma cell line (LLC1)-induced cancer cachexia in a mouse model. Specifically, GT rescued the lower levels of grip strength, hanging, and cross-sectional area caused by LLC1. Collectively, our findings suggest that GT may be a good therapeutic candidate for protecting against cancer cachexia.Yoseph Toni WijayaTania SetiawanIta Novita SariSeung-Yeol NahHyog Young KwonElsevierarticleGintoninMuscle atrophyCancer cachexiaOxidative stressNeoplasms. Tumors. Oncology. Including cancer and carcinogensRC254-282ENNeoplasia: An International Journal for Oncology Research, Vol 23, Iss 12, Pp 1307-1317 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Gintonin Muscle atrophy Cancer cachexia Oxidative stress Neoplasms. Tumors. Oncology. Including cancer and carcinogens RC254-282
spellingShingle	Gintonin Muscle atrophy Cancer cachexia Oxidative stress Neoplasms. Tumors. Oncology. Including cancer and carcinogens RC254-282 Yoseph Toni Wijaya Tania Setiawan Ita Novita Sari Seung-Yeol Nah Hyog Young Kwon Amelioration of muscle wasting by gintonin in cancer cachexia
description	Cancer cachexia is characterized by systemic inflammation, protein degradation, and loss of skeletal muscle. Despite extensive efforts to develop therapeutics, only few effective treatments are available to protect against cancer cachexia. Here, we found that gintonin (GT), a ginseng-derived lysophosphatidic acid receptor (LPAR) ligand, protected C2C12 myotubes from tumor necrosis factor α (TNFα)/interferon γ (IFNγ)- induced muscle wasting condition. The activity of GT was found to be dependent on LPAR/Gαi2, as the LPAR antagonist Ki16425 and Gαi2 siRNA abolished the anti-atrophic effects of GT on myotubes. GT suppressed TNFα-induced oxidative stress by reducing reactive oxygen species and suppressing inflammation-related genes, such as interleukin 6 (IL-6) and NADPH oxidase 2 (NOX-2). In addition, GT exhibited anti-atrophy effects in primary normal human skeletal myoblasts. Further, GT protected against Lewis lung carcinoma cell line (LLC1)-induced cancer cachexia in a mouse model. Specifically, GT rescued the lower levels of grip strength, hanging, and cross-sectional area caused by LLC1. Collectively, our findings suggest that GT may be a good therapeutic candidate for protecting against cancer cachexia.
format	article
author	Yoseph Toni Wijaya Tania Setiawan Ita Novita Sari Seung-Yeol Nah Hyog Young Kwon
author_facet	Yoseph Toni Wijaya Tania Setiawan Ita Novita Sari Seung-Yeol Nah Hyog Young Kwon
author_sort	Yoseph Toni Wijaya
title	Amelioration of muscle wasting by gintonin in cancer cachexia
title_short	Amelioration of muscle wasting by gintonin in cancer cachexia
title_full	Amelioration of muscle wasting by gintonin in cancer cachexia
title_fullStr	Amelioration of muscle wasting by gintonin in cancer cachexia
title_full_unstemmed	Amelioration of muscle wasting by gintonin in cancer cachexia
title_sort	amelioration of muscle wasting by gintonin in cancer cachexia
publisher	Elsevier
publishDate	2021
url	https://doaj.org/article/91368fd2de874bc5b0c3fd49f3a1625e
work_keys_str_mv	AT yosephtoniwijaya ameliorationofmusclewastingbygintoninincancercachexia AT taniasetiawan ameliorationofmusclewastingbygintoninincancercachexia AT itanovitasari ameliorationofmusclewastingbygintoninincancercachexia AT seungyeolnah ameliorationofmusclewastingbygintoninincancercachexia AT hyogyoungkwon ameliorationofmusclewastingbygintoninincancercachexia
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Amelioration of muscle wasting by gintonin in cancer cachexia

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