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The importance of acetyl coenzyme A synthetase for 11C-acetate uptake and cell survival in hepatocellular carcinoma

DC FieldValueLanguage
dc.contributor.author김경섭-
dc.contributor.author김재우-
dc.contributor.author윤미진-
dc.contributor.author이종두-
dc.date.accessioned2015-04-24T17:12:13Z-
dc.date.available2015-04-24T17:12:13Z-
dc.date.issued2009-
dc.identifier.issn0161-5505-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/104949-
dc.description.abstractWe analyzed the pattern of (11)C-acetate and (18)F-FDG uptake on PET/CT in patients with hepatocellular carcinoma (HCC). We also assessed the expression of important regulatory enzymes related to glycolysis and lipid synthesis in relation to (18)F-FDG and (11)C-acetate uptake in human HCC cell lines. The significance of (11)C-acetate uptake regulation was further evaluated with regard to cell viability. METHODS: (18)F-FDG and (11)C-acetate uptake patterns in HCC in 11 patients and in 5 HCC cell lines were assessed. We evaluated the gene expression of metabolic enzymes related to glycolysis and lipid synthesis in a cell line with the highest (18)F-FDG uptake and another cell line with the highest (11)C-acetate uptake. They included hexokinase II, adenosine triphosphate citrate lyase, acetyl coenzyme A (CoA) synthetase 1 (ACSS1), acetyl CoA synthetase 2 (ACSS2), acetyl CoA carboxylase, and fatty acid synthase. In a cell line with high (11)C-acetate uptake, the enzymatic activities of ACSS1 and ACSS2 were blocked using respective small, interfering RNAs (siRNAs), and the impact on (11)C-acetate uptake and cell viability was assessed. RESULTS: In all 11 patients and 4 of the 5 cell lines, the uptake patterns of the 2 radiotracers were complementary. ACSS1 and ACSS2 were highly expressed in a cell line with low (18)F-FDG uptake and high (11)C-acetate uptake, whereas only ACSS2 was expressed in a cell line with high (18)F-FDG uptake and low (11)C-acetate uptake. Fatty acid synthase expression was seen in cells with high (18)F-FDG or (11)C-acetate uptake. These findings indicate the possibility that both glucose and acetate can be a compensatory carbon source for lipid synthesis in cancer. Transient transfection with ACSS1 or ACSS2 siRNA in cells with high (11)C-acetate uptake decreased (11)C-acetate uptake and cell viability. CONCLUSION: The patterns of (18)F-FDG and (11)C-acetate uptake seemed to complement each other in both human HCC and HCC cell lines. Fatty acid synthase expression was seen in cells with high (18)F-FDG or (11)C-acetate uptake, suggesting glucose- or acetate-dependent lipid synthesis. Acetyl CoA synthetase appears to be important in (11)C-acetate uptake and acetate-dependent lipid synthesis for the growth of cancer cells with a low-glycolysis phenotype. Inhibition of acetyl CoA synthetase in these cells may be promising for anticancer treatment-
dc.description.statementOfResponsibilityopen-
dc.format.extent1222~1228-
dc.relation.isPartOfJournal of Nuclear Medicine-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.titleThe importance of acetyl coenzyme A synthetase for 11C-acetate uptake and cell survival in hepatocellular carcinoma-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Nuclear Medicine (핵의학)-
dc.contributor.googleauthorMijin Yun-
dc.contributor.googleauthorSeong-Hye Bang-
dc.contributor.googleauthorJae Woo Kim-
dc.contributor.googleauthorJun Young Park-
dc.contributor.googleauthorKyoung Sup Kim-
dc.contributor.googleauthorJong Doo Lee-
dc.identifier.doi10.2967/jnumed.109.062703-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA00297-
dc.contributor.localIdA00865-
dc.contributor.localIdA02550-
dc.contributor.localIdA03138-
dc.relation.journalcodeJ01644-
dc.contributor.alternativeNameKim, Kyung Sup-
dc.contributor.alternativeNameKim, Jae Woo-
dc.contributor.alternativeNameYun, Mi Jin-
dc.contributor.alternativeNameLee, Jong Doo-
dc.contributor.affiliatedAuthorKim, Kyung Sup-
dc.contributor.affiliatedAuthorKim, Jae Woo-
dc.contributor.affiliatedAuthorYun, Mi Jin-
dc.contributor.affiliatedAuthorLee, Jong Doo-
dc.citation.volume50-
dc.citation.number8-
dc.citation.startPage1222-
dc.citation.endPage1228-
dc.identifier.bibliographicCitationJournal of Nuclear Medicine, Vol.50(8) : 1222-1228, 2009-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Nuclear Medicine (핵의학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Biochemistry and Molecular Biology (생화학-분자생물학교실) > 1. Journal Papers

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