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  1. 原著論文

Cytosolic acetyl-CoA synthetase affected tumor cell survival under hypoxia: the possible function in tumor acetyl-CoA/acetate metabolism

https://repo.qst.go.jp/records/46122
https://repo.qst.go.jp/records/46122
13c6e3a9-2e50-4662-9584-2188f30287d5
Item type 学術雑誌論文 / Journal Article(1)
公開日 2011-07-06
タイトル
タイトル Cytosolic acetyl-CoA synthetase affected tumor cell survival under hypoxia: the possible function in tumor acetyl-CoA/acetate metabolism
言語
言語 eng
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 metadata only access
アクセス権URI http://purl.org/coar/access_right/c_14cb
著者 Yoshii, Yukie

× Yoshii, Yukie

WEKO 459181

Yoshii, Yukie

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Furukawa, Takako

× Furukawa, Takako

WEKO 459182

Furukawa, Takako

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Kiyono, Yashushi

× Kiyono, Yashushi

WEKO 459183

Kiyono, Yashushi

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Yonekura, Yoshiharu

× Yonekura, Yoshiharu

WEKO 459184

Yonekura, Yoshiharu

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Fujibayashi, Yasuhisa

× Fujibayashi, Yasuhisa

WEKO 459185

Fujibayashi, Yasuhisa

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et.al

× et.al

WEKO 459186

et.al

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吉井 幸恵

× 吉井 幸恵

WEKO 459187

en 吉井 幸恵

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古川 高子

× 古川 高子

WEKO 459188

en 古川 高子

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米倉 義晴

× 米倉 義晴

WEKO 459189

en 米倉 義晴

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藤林 康久

× 藤林 康久

WEKO 459190

en 藤林 康久

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内容記述タイプ Abstract
内容記述 Understanding tumor-specific metabolism under hypoxia is important to find novel targets for antitumor drug design. Here we found that tumor cells expressed higher levels of cytosolic acetyl-CoA synthetase (ACSS2) under hypoxia than normoxia. Knockdown of ACSS2 by RNA interference (RNAi) in tumor cells enhanced tumor cell death under long-term hypoxia in vitro. Our data also demonstrated that the ACSS2 suppression slowed tumor growth in vivo. These findings showed that ACSS2 plays a significant role in tumor cell survival under hypoxia and that ACSS2 would be a potential target for tumor treatment. Furthermore, we found that tumor cells excreted acetate and the quantity increased under hypoxia: the pattern of acetate excretion followed the expression pattern of ACSS2. Additionally, the ACSS2 knockdown led to a corresponding reduction in the acetate excretion in tumor cells. These results mean that ACSS2 can conduct the reverse reaction from acetyl-CoA to acetate in tumor cells, which indicates that ACSS2 is a bi-directional enzyme in tumor cells and that ACSS2 might play a buffering role in tumor acetyl-CoA/acetate metabolism.
書誌情報 Cancer Science

巻 100, 号 5, p. 821-827, 発行日 2009-02
ISSN
収録物識別子タイプ ISSN
収録物識別子 1347-9032
DOI
識別子タイプ DOI
関連識別子 10.1111/j.1349-7006.2009.01099.x
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