Involvement of fatty acid-CoA ligase 4 in hepatocellular carcinoma growth: Roles of cyclic AMP and p38 mitogen-activated protein kinase

Yu Chih Liang, Chih Hsiung Wu, Jan Show Chu, Chung Kwe Wang, Ling Fang Hung, Ying Jan Wang, Yuan Soon Ho, Jan Gowth Chang, Shyr Yi Lin

研究成果: 雜誌貢獻文章

27 引文 (Scopus)

摘要

Aim: Fatty acid-CoA ligase 4 (FACL4) is an arachidonate-Preferring enzyme which has been shown to be up-regulated in human colon cancer tissues and implicated in the colon tumorigenesis. The purpose of this study was to investigate the role of FACL4 in the human hepatocellular carcinoma (HCC) tumorigenesis and the specific signal pathways involved in this process. Methods: We investigated the expression and regulation of FACL4 in HCC, adjacent non-tumorous liver tissues, and cell lines. Results: In HCC patients, we demonstrated that FACL4 gene expression was markedly elevated in the cancerous tissues than in the adjacent non-cancerous liver tissues. In addition, several human hepatoma cell lines, including Hep3B and HepG2, expressed high levels of FACL4. Stable overex-pression of FACL4 knockdown plasmids (small interfering RNA, siRNA) to Hep3B cells significantly decreased FACL4 expression and subsequently limited the cell proliferation. Treatment of Hep3B cells with 8-bromo-cAMP and SB203508 (p38 MAPK inhibitor) significantly suppressed the FACL4 expression. Conclusion: FACL4 is involved in the HCC tumorigenesis and both cAMP and p38 MAPK pathways are associated with the regulation of FACL4 in HCC.
原文英語
頁(從 - 到)2557-2563
頁數7
期刊World Journal of Gastroenterology
11
發行號17
出版狀態已發佈 - 五月 7 2005

指紋

p38 Mitogen-Activated Protein Kinases
Coenzyme A
Ligases
Cyclic AMP
Hepatocellular Carcinoma
Fatty Acids
Growth
Carcinogenesis
8-Bromo Cyclic Adenosine Monophosphate
Cell Line
Liver
Colonic Neoplasms
Small Interfering RNA
Signal Transduction
Colon
Plasmids
Cell Proliferation
Gene Expression

ASJC Scopus subject areas

  • Gastroenterology

引用此文

Involvement of fatty acid-CoA ligase 4 in hepatocellular carcinoma growth : Roles of cyclic AMP and p38 mitogen-activated protein kinase. / Liang, Yu Chih; Wu, Chih Hsiung; Chu, Jan Show; Wang, Chung Kwe; Hung, Ling Fang; Wang, Ying Jan; Ho, Yuan Soon; Chang, Jan Gowth; Lin, Shyr Yi.

於: World Journal of Gastroenterology, 卷 11, 編號 17, 07.05.2005, p. 2557-2563.

研究成果: 雜誌貢獻文章

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title = "Involvement of fatty acid-CoA ligase 4 in hepatocellular carcinoma growth: Roles of cyclic AMP and p38 mitogen-activated protein kinase",
abstract = "Aim: Fatty acid-CoA ligase 4 (FACL4) is an arachidonate-Preferring enzyme which has been shown to be up-regulated in human colon cancer tissues and implicated in the colon tumorigenesis. The purpose of this study was to investigate the role of FACL4 in the human hepatocellular carcinoma (HCC) tumorigenesis and the specific signal pathways involved in this process. Methods: We investigated the expression and regulation of FACL4 in HCC, adjacent non-tumorous liver tissues, and cell lines. Results: In HCC patients, we demonstrated that FACL4 gene expression was markedly elevated in the cancerous tissues than in the adjacent non-cancerous liver tissues. In addition, several human hepatoma cell lines, including Hep3B and HepG2, expressed high levels of FACL4. Stable overex-pression of FACL4 knockdown plasmids (small interfering RNA, siRNA) to Hep3B cells significantly decreased FACL4 expression and subsequently limited the cell proliferation. Treatment of Hep3B cells with 8-bromo-cAMP and SB203508 (p38 MAPK inhibitor) significantly suppressed the FACL4 expression. Conclusion: FACL4 is involved in the HCC tumorigenesis and both cAMP and p38 MAPK pathways are associated with the regulation of FACL4 in HCC.",
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author = "Liang, {Yu Chih} and Wu, {Chih Hsiung} and Chu, {Jan Show} and Wang, {Chung Kwe} and Hung, {Ling Fang} and Wang, {Ying Jan} and Ho, {Yuan Soon} and Chang, {Jan Gowth} and Lin, {Shyr Yi}",
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T1 - Involvement of fatty acid-CoA ligase 4 in hepatocellular carcinoma growth

T2 - Roles of cyclic AMP and p38 mitogen-activated protein kinase

AU - Liang, Yu Chih

AU - Wu, Chih Hsiung

AU - Chu, Jan Show

AU - Wang, Chung Kwe

AU - Hung, Ling Fang

AU - Wang, Ying Jan

AU - Ho, Yuan Soon

AU - Chang, Jan Gowth

AU - Lin, Shyr Yi

PY - 2005/5/7

Y1 - 2005/5/7

N2 - Aim: Fatty acid-CoA ligase 4 (FACL4) is an arachidonate-Preferring enzyme which has been shown to be up-regulated in human colon cancer tissues and implicated in the colon tumorigenesis. The purpose of this study was to investigate the role of FACL4 in the human hepatocellular carcinoma (HCC) tumorigenesis and the specific signal pathways involved in this process. Methods: We investigated the expression and regulation of FACL4 in HCC, adjacent non-tumorous liver tissues, and cell lines. Results: In HCC patients, we demonstrated that FACL4 gene expression was markedly elevated in the cancerous tissues than in the adjacent non-cancerous liver tissues. In addition, several human hepatoma cell lines, including Hep3B and HepG2, expressed high levels of FACL4. Stable overex-pression of FACL4 knockdown plasmids (small interfering RNA, siRNA) to Hep3B cells significantly decreased FACL4 expression and subsequently limited the cell proliferation. Treatment of Hep3B cells with 8-bromo-cAMP and SB203508 (p38 MAPK inhibitor) significantly suppressed the FACL4 expression. Conclusion: FACL4 is involved in the HCC tumorigenesis and both cAMP and p38 MAPK pathways are associated with the regulation of FACL4 in HCC.

AB - Aim: Fatty acid-CoA ligase 4 (FACL4) is an arachidonate-Preferring enzyme which has been shown to be up-regulated in human colon cancer tissues and implicated in the colon tumorigenesis. The purpose of this study was to investigate the role of FACL4 in the human hepatocellular carcinoma (HCC) tumorigenesis and the specific signal pathways involved in this process. Methods: We investigated the expression and regulation of FACL4 in HCC, adjacent non-tumorous liver tissues, and cell lines. Results: In HCC patients, we demonstrated that FACL4 gene expression was markedly elevated in the cancerous tissues than in the adjacent non-cancerous liver tissues. In addition, several human hepatoma cell lines, including Hep3B and HepG2, expressed high levels of FACL4. Stable overex-pression of FACL4 knockdown plasmids (small interfering RNA, siRNA) to Hep3B cells significantly decreased FACL4 expression and subsequently limited the cell proliferation. Treatment of Hep3B cells with 8-bromo-cAMP and SB203508 (p38 MAPK inhibitor) significantly suppressed the FACL4 expression. Conclusion: FACL4 is involved in the HCC tumorigenesis and both cAMP and p38 MAPK pathways are associated with the regulation of FACL4 in HCC.

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