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Acetate production: a possible tumor specific metabolic pathway to survive hypoxia
https://repo.qst.go.jp/records/65107
https://repo.qst.go.jp/records/65107749452c9-ad3c-4e75-8d88-3636b016e34f
| Item type | 会議発表用資料 / Presentation(1) | |||||
|---|---|---|---|---|---|---|
| 公開日 | 2013-08-23 | |||||
| タイトル | ||||||
| タイトル | Acetate production: a possible tumor specific metabolic pathway to survive hypoxia | |||||
| 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_c94f | |||||
| 資源タイプ | conference object | |||||
| 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 |
Furukawa, Takako
× Furukawa, Takako× Yoshii, Yukie× Fujibayashi, Yasuhisa× 古川 高子× 藤林 康久 |
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| 抄録 | ||||||
| 内容記述タイプ | Abstract | |||||
| 内容記述 | Tumor cells are known to exhibit high levels of glycolysis and low levels of mitochondrial oxidative phosphorylation, even in the presence of oxygen. The high levels of glycolysis lead to increased lactate production under hypoxia but it is not always the case under normoxia. This phenomenon prompted us to speculate that tumor cells might possess tumor-specific pathways to break down pyruvate, the final product of glycolysis. While investigating tumor specific metabolites, we found that tumor cells excreted acetate under normoxia and the quantity increased under hypoxia. The acetate production followed the expression pattern of cytosolic acetyl-CoA synthetase (Acss2), an enzyme fixing acetate into acetyl-CoA using ATP. Knockdown of Acss2 by RNA interference (RNAi) led to a corresponding reduction in acetate production in tumor cells, indicating that Acss2 is conducting the reverse reaction converting acetyl-CoA into acetate with ATP synthesis. In Acss2-RNAi tumor cells, the cellular ATP levels tended to be lower than the control-RNAi tumor cells. These results suggest that Acss2 might be controlling both anabolism and catabolism of acetate coordinately to maintain the metabolic balance in tumor cells. Furthermore, Acss2 knockdown decreased cell survival under long-term hypoxia in vitro and slowed tumor growth in vivo, indicating that Acss2 plays a significant role in tumor survival under hypoxia. | |||||
| 会議概要（会議名, 開催地, 会期, 主催者等） | ||||||
| 内容記述タイプ | Other | |||||
| 内容記述 | Kashiwa Symposium on Cancer Biology 2008 | |||||
| 発表年月日 | ||||||
| 日付 | 2008-11-14 | |||||
| 日付タイプ | Issued | |||||
