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Is acetate metabolism a possible imaging marker for hypoxia-stimulating tumors?
https://repo.qst.go.jp/records/71223
https://repo.qst.go.jp/records/71223097f5586-644c-44ee-a9da-42383c4252d1
| Item type | 会議発表用資料 / Presentation(1) | |||||
|---|---|---|---|---|---|---|
| 公開日 | 2013-08-29 | |||||
| タイトル | ||||||
| タイトル | Is acetate metabolism a possible imaging marker for hypoxia-stimulating tumors? | |||||
| 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 |
Yoshii, Yukie
× Yoshii, Yukie× Furukawa, Takako× Yoshii, Hiroshi× 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 | Our previous study showed that acetate fixation into lipids is elevated in tumor cells: this characteristic underlies 11C-acetate PET of tumors. The pathway is considered to be driven by acetyl-CoA synthetase (Acss) converting acetate to acetyl-CoA. On the other hand, we found that tumor cells can also utilize a reverse reaction of Acss for ATP synthesis through acetate production, which resembles known pathway in ancient anaerobic organisms. These facts collectively point out that Acss manages both anabolism and catabolism of acetate coordinately in tumor cells. Additionally, we found that expression of Acss was increased significantly under hypoxia, which indicates that total activity of acetate metabolism is up-regulated in hypoxic tumor cells. In this study, to confirm the above supposition and propose acetate PET as a new tumor metabolic imaging, we examined the characteristics of tumor acetate uptake under hypoxia. We performed 14C-acetate uptake study using cultured mouse tumor cells in 24-well plates with fibroblast cells as control. Cells were incubated under normoxia for 24 h, then a part of them were treated by 2 h hypoxia. After preincubation, medium containing 1mu Ci 14C-acetate was added to each well and the cells were further incubated for 1 h under the same condition. After cell lyses, radioactivity was measured by a liquid scintillation counter. To verify the role of Acss, we also examined 14C-acetate uptake in Acss-knockdown tumor cells. Our data demonstrated that 14C-acetate uptake was higher under hypoxia than normoxia in tumor cells, but not in normal cells, and that knock down of Acss decreased 14C-acetate uptake in tumor cells. Based on these results, we concluded that tumor acetate metabolism mediated by Acss was up-regulated under hypoxia, which caused the increase of 14C-acetate uptake. These findings suggest a possibility that 11C-acetate PET is visualizing hypoxia-stimulated up-regulation of acetate metabolism in tumor cells. |
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| 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 | Joint Molecular Imaging Conference | |||||
| 発表年月日 | ||||||
| 日付 | 2007-09-11 | |||||
| 日付タイプ | Issued | |||||
