Liver Cancer
Copyright ©2005 Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. May 7, 2005; 11(17): 2557-2563
Published online May 7, 2005. doi: 10.3748/wjg.v11.i17.2557
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
Yu-Chih Liang, Ling-Fang Hung, Yuan-Soon Ho, School of Medical Technology, Taipei Medical University, Taipei, Taiwan, China
Chih-Hsiung Wu, Department of Surgery, Taipei Medical University Hospital, Taipei Medical University, Taipei, Taiwan, China
Jan-Show Chu, Department of Pathology, School of Medicine, Taipei Medical University, Taipei, Taiwan, China
Chung-Kwe Wang, Department of Internal Medicine, Taipei Municipal Jen-Ai Hospital, Taipei, Taiwan, China
Ying-Jan Wang, Department of Environmental and Occupational Health, National Cheng Kung University Medical College, Tainan, Taiwan, China
Jan-Gowth Chang, Department of Molecular Medicine and Laboratory Medicine, China Medical University Hospital, Taiwan, China
Shyr-Yi Lin, Department of Internal Medicine, School of Medicine; Department of Internal Medicine, Taipei Medical University Hospital, Taipei Medical University, Taipei, Taiwan, China
Author contributions: All authors contributed equally to the work.
Correspondence to: Dr. Shyr-Yi Lin, Taipei Medical University, 250 Wu-Hsing Street, Taipei 110, Taiwan, China. sylin@tmu.edu.tw
Telephone: +886-2-27361661-3210 Fax: +886-2-27393447
Received: June 24, 2004
Revised: June 25, 2004
Accepted: July 17, 2004
Published online: May 7, 2005
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.

Keywords: FACL-4, HCC