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  1. 20 医学系研究科・医学部
  2. 20A 学術誌論文
  3. 20A1 雑誌掲載論文

Macrophage inhibitory cytokine-1 induced by a high-fat diet promotes prostate cancer progression by stimulating tumor-promoting cytokine production from tumor stromal cells

http://hdl.handle.net/10295/00006171
http://hdl.handle.net/10295/00006171
2646e442-d715-4ff3-9e6b-edf5c867a937
名前 / ファイル ライセンス アクション
iA_2022_36.pdf iA_2022_36.pdf (3.6 MB)
Item type 学術雑誌論文 / Journal Article(1)
公開日 2023-02-19
タイトル
タイトル Macrophage inhibitory cytokine-1 induced by a high-fat diet promotes prostate cancer progression by stimulating tumor-promoting cytokine production from tumor stromal cells
言語 en
言語
言語 eng
主題
主題Scheme Other
主題 macrophage inhibitory cytokine&#8208
主題
主題Scheme Other
主題 1
主題
主題Scheme Other
主題 tumor microenvironment
主題
主題Scheme Other
主題 high&#8208
主題
主題Scheme Other
主題 fat diet
主題
主題Scheme Other
主題 prostate cancer
主題
主題Scheme Other
主題 metabolism
資源タイプ
資源タイプ識別子 http://purl.org/coar/resource_type/c_6501
資源タイプ journal article
アクセス権
アクセス権 open access
アクセス権URI http://purl.org/coar/access_right/c_abf2
作成者 Huang, Mingguo

× Huang, Mingguo

en Huang, Mingguo

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Narita, Shintaro

× Narita, Shintaro

en Narita, Shintaro

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Koizumi, Atsushi

× Koizumi, Atsushi

en Koizumi, Atsushi

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Nara, Taketoshi

× Nara, Taketoshi

en Nara, Taketoshi

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Numakura, Kazuyuki

× Numakura, Kazuyuki

en Numakura, Kazuyuki

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Satoh, Shigeru

× Satoh, Shigeru

en Satoh, Shigeru

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Nanjo, Hiroshi

× Nanjo, Hiroshi

en Nanjo, Hiroshi

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Habuchi, Tomonori

× Habuchi, Tomonori

en Habuchi, Tomonori

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内容記述
内容記述タイプ Abstract
内容記述 Background Recent studies have indicated that a high-fat diet (HFD) and/or HFD-induced obesity may influence prostate cancer (PCa) progression, but the role of HFD in PCa microenvironment is unclear. This study aimed to delineate the molecular mechanisms of PCa progression under HFD milieus and define the stromal microenvironment focusing on macrophage inhibitory cytokine-1 (MIC-1) activation. Methods We investigated the effects of HFD on PCa stromal microenvironment and MIC-1 signaling activation using PC-3M-luc-C6 PCa model mice fed with HFD or control diet. Further, we explored the effect of periprostatic adipocytes derived from primary PCa patients on activation and cytokine secretion of prostate stromal fibroblasts. Expression patterns and roles of MIC-1 signaling on human PCa stroma activation and progression were also investigated. Results HFD stimulated PCa cell growth and invasion as a result of upregulated MIC-1 signaling and subsequently increased the secretion of interleukin (IL)-8 and IL-6 from prostate stromal fibroblasts in PC-3M-luc-C6 PCa mouse model. In addition, periprostatic adipocytes directly stimulated MIC-1 production from PC-3 cells and IL-8 secretion in prostate stromal fibroblasts through the upregulation of adipose lipolysis and free fatty acid release. The increased serum MIC-1 was significantly correlated with human PCa stroma activation, high serum IL-8, IL-6, and lipase activity, advanced PCa progression, and high body mass index of the patients. Glial-derived neurotrophic factor receptor alpha-like (GFRAL), a specific receptor of MIC-1, was highly expressed in both cytoplasm and membrane of PCa cells and surrounding stromal fibroblasts, and the expression level was decreased by androgen deprivation therapy and chemotherapy. Conclusion HFD-mediated activation of the PCa stromal microenvironment through metabolically upregulated MIC-1 signaling by increased available free fatty acids may be a critical mechanism of HFD and/or obesity-induced PCa progression.
言語 en
出版タイプ
出版タイプ VoR
出版タイプResource http://purl.org/coar/version/c_970fb48d4fbd8a85
書誌情報 en : Cancer Communications

巻 41, 号 5, p. 389-403, 発行日 2021
収録物識別子
収録物識別子タイプ ISSN
収録物識別子 2523-3548
出版者
出版者 John Wiley and Sons Inc
関連情報
関連タイプ isIdenticalTo
識別子タイプ DOI
関連識別子 https://doi.org/10.1002/cac2.12137
権利情報
権利情報 This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. © 2021 The Authors. Cancer Communications published by JohnWiley & Sons Australia, Ltd. on behalf of Sun Yat-sen University Cancer Center
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