Fatty acid metabolic enzyme acyl-CoA thioesterase 8 promotes the development of hepatocellular carcinoma

Y. U.Hsuan Hung, Y. I.Shin Chan, Yung Sheng Chang, Kuo Ting Lee, Hui Ping Hsu, Meng Chi Yen, Wei Ching Chen, Chih Yang Wang, Ming Derg Lai

研究成果: 雜誌貢獻文章

11 引文 (Scopus)

摘要

Dysregulated metabolism is an emerging hallmark of cancer development, and upregulated lipid synthesis is one of the important tumor metabolic features. However, lipolysis may also contribute to cancer pathogenesis by altering free fatty acid (FFA) metabolism. In the present study, we investigated the importance of the lipolytic enzyme acyl-CoA thioesterase 8 (ACOT8) in hepatocellular carcinoma (HCC) development. Bioinformatic analysis of published microarrays regarding clinical specimens revealed that both ACOT8 gene copy number and mRNA expression were increased in HCC tissues when compared to these variables in non-tumor tissues. ACOT8 silencing with specific shRNA stably expressed in Huh7 and Hep3B HCC cell lines showed that ACOT8 protein expression and overall thioesterase activity were reduced following ACOT8 knockdown. In vitro tumorigenic assays revealed that ACOT8 knockdown inhibited anchorage-dependent and -independent growth of HCC cell lines. This growth inhibition was partially rescued by addition of the FFA, myristic acid, indicating the importance of FFA in cancer metabolism. In summary, lipolytic enzyme ACOT8 is frequently upregulated in HCC clinical specimens. More importantly, ACOT8 silencing leads to inhibition of cell growth in HCC in vitro.
原文英語
頁(從 - 到)2797-2803
頁數7
期刊Oncology Reports
31
發行號6
DOIs
出版狀態已發佈 - 一月 1 2014
對外發佈Yes

指紋

Neoplastic Gene Expression Regulation
Palmitoyl-CoA Hydrolase
Acyl Coenzyme A
Hep G2 Cells
Liver Neoplasms
Proteomics
Hepatocellular Carcinoma
Fatty Acids
Cell Proliferation
Messenger RNA
Enzymes
Nonesterified Fatty Acids
Neoplasms
Growth
Cell Line
Gene Dosage
Lipolysis
Myristic Acid
Microarray Analysis
Computational Biology

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

引用此文

Hung, Y. U. H., Chan, Y. I. S., Chang, Y. S., Lee, K. T., Hsu, H. P., Yen, M. C., ... Lai, M. D. (2014). Fatty acid metabolic enzyme acyl-CoA thioesterase 8 promotes the development of hepatocellular carcinoma. Oncology Reports, 31(6), 2797-2803. https://doi.org/10.3892/or.2014.3155

Fatty acid metabolic enzyme acyl-CoA thioesterase 8 promotes the development of hepatocellular carcinoma. / Hung, Y. U.Hsuan; Chan, Y. I.Shin; Chang, Yung Sheng; Lee, Kuo Ting; Hsu, Hui Ping; Yen, Meng Chi; Chen, Wei Ching; Wang, Chih Yang; Lai, Ming Derg.

於: Oncology Reports, 卷 31, 編號 6, 01.01.2014, p. 2797-2803.

研究成果: 雜誌貢獻文章

Hung, YUH, Chan, YIS, Chang, YS, Lee, KT, Hsu, HP, Yen, MC, Chen, WC, Wang, CY & Lai, MD 2014, 'Fatty acid metabolic enzyme acyl-CoA thioesterase 8 promotes the development of hepatocellular carcinoma', Oncology Reports, 卷 31, 編號 6, 頁 2797-2803. https://doi.org/10.3892/or.2014.3155
Hung, Y. U.Hsuan ; Chan, Y. I.Shin ; Chang, Yung Sheng ; Lee, Kuo Ting ; Hsu, Hui Ping ; Yen, Meng Chi ; Chen, Wei Ching ; Wang, Chih Yang ; Lai, Ming Derg. / Fatty acid metabolic enzyme acyl-CoA thioesterase 8 promotes the development of hepatocellular carcinoma. 於: Oncology Reports. 2014 ; 卷 31, 編號 6. 頁 2797-2803.
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abstract = "Dysregulated metabolism is an emerging hallmark of cancer development, and upregulated lipid synthesis is one of the important tumor metabolic features. However, lipolysis may also contribute to cancer pathogenesis by altering free fatty acid (FFA) metabolism. In the present study, we investigated the importance of the lipolytic enzyme acyl-CoA thioesterase 8 (ACOT8) in hepatocellular carcinoma (HCC) development. Bioinformatic analysis of published microarrays regarding clinical specimens revealed that both ACOT8 gene copy number and mRNA expression were increased in HCC tissues when compared to these variables in non-tumor tissues. ACOT8 silencing with specific shRNA stably expressed in Huh7 and Hep3B HCC cell lines showed that ACOT8 protein expression and overall thioesterase activity were reduced following ACOT8 knockdown. In vitro tumorigenic assays revealed that ACOT8 knockdown inhibited anchorage-dependent and -independent growth of HCC cell lines. This growth inhibition was partially rescued by addition of the FFA, myristic acid, indicating the importance of FFA in cancer metabolism. In summary, lipolytic enzyme ACOT8 is frequently upregulated in HCC clinical specimens. More importantly, ACOT8 silencing leads to inhibition of cell growth in HCC in vitro.",
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AU - Hsu, Hui Ping

AU - Yen, Meng Chi

AU - Chen, Wei Ching

AU - Wang, Chih Yang

AU - Lai, Ming Derg

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AB - Dysregulated metabolism is an emerging hallmark of cancer development, and upregulated lipid synthesis is one of the important tumor metabolic features. However, lipolysis may also contribute to cancer pathogenesis by altering free fatty acid (FFA) metabolism. In the present study, we investigated the importance of the lipolytic enzyme acyl-CoA thioesterase 8 (ACOT8) in hepatocellular carcinoma (HCC) development. Bioinformatic analysis of published microarrays regarding clinical specimens revealed that both ACOT8 gene copy number and mRNA expression were increased in HCC tissues when compared to these variables in non-tumor tissues. ACOT8 silencing with specific shRNA stably expressed in Huh7 and Hep3B HCC cell lines showed that ACOT8 protein expression and overall thioesterase activity were reduced following ACOT8 knockdown. In vitro tumorigenic assays revealed that ACOT8 knockdown inhibited anchorage-dependent and -independent growth of HCC cell lines. This growth inhibition was partially rescued by addition of the FFA, myristic acid, indicating the importance of FFA in cancer metabolism. In summary, lipolytic enzyme ACOT8 is frequently upregulated in HCC clinical specimens. More importantly, ACOT8 silencing leads to inhibition of cell growth in HCC in vitro.

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