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.
| Original language | English |
|---|---|
| Pages (from-to) | 2557-2563 |
| Number of pages | 7 |
| Journal | World Journal of Gastroenterology |
| Volume | 11 |
| Issue number | 17 |
| Publication status | Published - May 7 2005 |
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Keywords
- FACL-4
- HCC
ASJC Scopus subject areas
- Gastroenterology
Cite this
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.
In: World Journal of Gastroenterology, Vol. 11, No. 17, 07.05.2005, p. 2557-2563.Research output: Contribution to journal › Article
}
TY - JOUR
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.
KW - FACL-4
KW - HCC
UR - http://www.scopus.com/inward/record.url?scp=18944392165&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=18944392165&partnerID=8YFLogxK
M3 - Article
C2 - 15849811
AN - SCOPUS:18944392165
VL - 11
SP - 2557
EP - 2563
JO - World Journal of Gastroenterology
JF - World Journal of Gastroenterology
SN - 1007-9327
IS - 17
ER -