Tumor uptake of radiolabeled acetate reflects the expression of cytosolic acetyl-CoA synthetase: implications for the mechanism of acetate PET
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Introduction: [1-^<11>C]acetate positron emission tomography (PET) is used for myocardialstudies. In the myocardium, mitochondrial acetyl-CoA synthetase (ACSS1) mainlycontributes to the radiopharmaceutical uptake. [1-^<11>C]acetate PET is also used for tumordiagnosis; however, the uptake mechanism of radiolabeled acetate in tumors remains unclear.Our previous study reported that cytosolic acetyl-CoA synthetase (ACSS2) was expressed intumor cells and up-regulated under hypoxia; whereas, expression of ACSS1 was negligibleregardless of the oxygen conditions. We also indicated that ACSS2 is a bi-directional enzymethat controls acetyl-CoA / acetate metabolism in tumor cells. In this study, to elucidate thebasic mechanism of tumor acetate uptake, we focused on ACSS2 and investigated the role ofACSS2 in the uptake of radiolabeled acetate in tumor cells. Methods: [1-^<14>C]acetate uptake and ACSS2 expression were examined in four tumor celllines 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 patternfollowed that of ACSS2 expression. The incorporated ^<14>C was mostly distributed in thelipid-soluble fractions, and this tendency increased under hypoxia. ACSS2 knock down led toa corresponding reduction in [1-^<14>C]acetate uptake in all tumor cell lines examined undernormoxia and hypoxia. Conclusions: ACSS2 plays an important role in the uptake of radiolabeled acetate in tumorcells, which is different from that in the myocardium, which mainly involves ACSS1. Theuptake of radiolabeled acetate in tumors increased under hypoxia along with up-regulation ofACSS2 expression. This suggests a possible mechanism for acetate PET for tumors.
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