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

作     者：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 

作者机构：School of Medical Technology Taipei Medical UniversityTaipeiTaiwanChina Department of Surgery Taipei Medical University HospitalTaipei Medical UniversityTaipeiTaiwanChina Department of Pathology School of MedicineTaipei Medical UniversityTaipeiTaiwanChina Department of Internal Medicine Taipei Municipal Jen-Ai HospitalTaipeiTaiwanChina Department of Environmental and Occupational Health National Cheng Kung University Medical CollegeTainanTaiwanChina Department of Molecular Medicine and Laboratory Medicine China Medical University HospitalTaiwanChina Department of Internal Medicine School of Medicine Department of Internal MedicineTaipei Medical University HospitalTaipei Medical UniversityTaipeiTaiwanChina 

出 版 物：《World Journal of Gastroenterology》 (世界胃肠病学杂志（英文版）)

年 卷 期：2005年第11卷第17期

页      面：2557-2563页

核心收录：

学科分类：1002[医学-临床医学] 100214[医学-肿瘤学] 10[医学] 

基　　金：Supported by the National Science Council of Taiwan Chna(NSC 91-2320-B-038-030- and 92-2320-B-038-051-)Taipei Medical University (TMU 91-Y05-A138) 

主　　题：FACL-4 HCC 

摘      要：AIM: Fatty acid-CoA ligase 4 (FACL4) is an arachidonatepreferring 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 investigatethe role of FACL4 in the human hepatocellular carcinoma (HCC) tumorigenesis and the specific signal pathways involved in this ***: We investigated the expression and regulation of FACL4 in HCC, adjacent non-tumorous liver tissues, and cell ***: In HCC patients, we demonstrated that FACL4 gene expression was markedly elevated in the cancerous tissues than in the adjacent non-cancerous liver *** 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 8bromo-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.