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Please use this identifier to cite or link to this item: http://hdl.handle.net/10098/2403

タイトル: Tumor uptake of radiolabeled acetate reflects the expression of cytosolic acetyl-CoA synthetase: implications for the mechanism of acetate PET
著者: YOSHII, Yukie
WAKI, Atsuo
KIYONO, Yasushi
MORI, Tetsuya
YOSHII, Hiroshi
KUDO, Takashi
OKAZAWA, Hidehiko
WELCH, Michael J.
キーワード: Acetate
Acetyl-CoA synthetase
Issue Date: Oct-2009
抄録: Introduction: [1-^<11>C]acetate positron emission tomography (PET) is used for myocardial studies. In the myocardium, mitochondrial acetyl-CoA synthetase (ACSS1) mainly contributes to the radiopharmaceutical uptake. [1-^<11>C]acetate PET is also used for tumor diagnosis; however, the uptake mechanism of radiolabeled acetate in tumors remains unclear. Our previous study reported that cytosolic acetyl-CoA synthetase (ACSS2) was expressed in tumor cells and up-regulated under hypoxia; whereas, expression of ACSS1 was negligible regardless of the oxygen conditions. We also indicated that ACSS2 is a bi-directional enzyme that controls acetyl-CoA / acetate metabolism in tumor cells. In this study, to elucidate the basic mechanism of tumor acetate uptake, we focused on ACSS2 and investigated the role of ACSS2 in the uptake of radiolabeled acetate in tumor cells. Methods: [1-^<14>C]acetate uptake and ACSS2 expression were examined in four tumor cell lines under normoxia or hypoxia. An ACSS2 knockdown study was also performed. Results: [1-^<14>C]acetate uptake was increased in the tumor cells under hypoxia. This pattern followed that of ACSS2 expression. The incorporated ^<14>C was mostly distributed in the lipid-soluble fractions, and this tendency increased under hypoxia. ACSS2 knock down led to a corresponding reduction in [1-^<14>C]acetate uptake in all tumor cell lines examined under normoxia and hypoxia. Conclusions: ACSS2 plays an important role in the uptake of radiolabeled acetate in tumor cells, which is different from that in the myocardium, which mainly involves ACSS1. The uptake of radiolabeled acetate in tumors increased under hypoxia along with up-regulation of ACSS2 expression. This suggests a possible mechanism for acetate PET for tumors.
URI: http://hdl.handle.net/10098/2403
ISSN: 09698051
Appears in Collections:07 高エネルギー医学研究センター
01-770 雑誌等掲載論文

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