Abstract：
AIMS:Cyclooxygenase-2 (COX-2)-controlled production of prostaglandin E(2) (PGE(2)) has been implicated in cell growth and metastasis in many cancers. Recent studies have found that COX-2 is co-expressed with survivin in many cancers. Survivin is a member of the inhibitor-of-apoptosis protein family. Some COX-2 inhibitors (e.g., celecoxib) can reduce the expression of survivin. However, little is known about the mechanism of PGE(2)-mediated expression of survivin. This study was designed to uncover the effect of PGE(2) on survivin expression in hepatocellular carcinoma cells. MAIN METHODS:The effects of PGE(2) and EP1 agonist on survivin expression were examined in HUH-7 and HepG2 cells. Plasmid transfection and EP1 siRNA were used to regulate the expression of COX-2 and the EP1 receptor protein. KEY FINDINGS:PGE(2) treatment increased survivin expression 2.3-fold. COX-2 overexpression resulted in a similar level of survivin upregulation. However, this effect was suppressed by treatment with celecoxib. EP1 receptor transfection or treatment with a selective EP1 agonist mimicked the effect of PGE(2) treatment. Conversely, the PGE(2)-induced upregulation of survivin was blocked by treatment with a selective EP1 antagonist or siRNA against the EP1 receptor. The phosphorylation of EGFR and Akt were elevated in EP1 agonist-treated cells, and both EGFR and PI3K inhibitors suppressed the upregulation of survivin induced by PGE(2) or EP1 agonist. SIGNIFICANCE:PGE(2) regulates survivin expression in hepatocellular carcinoma cells through the EP1 receptor by activating the EGFR/PI3K pathway. Targeting the PGE(2)/EP1/survivin signaling pathway may aid the development of new therapeutic strategies for both the prevention and treatment of this cancer.
journal_name
Life Scijournal_title
Life sciencesauthors
Bai XM,Jiang H,Ding JX,Peng T,Ma J,Wang YH,Zhang L,Zhang H,Leng Jdoi
10.1016/j.lfs.2009.12.009subject
Has Abstractpub_date
2010-01-30 00:00:00pages
214-23issue
5-6eissn
0024-3205issn
1879-0631pii
S0024-3205(09)00509-8journal_volume
86pub_type
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