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Cordycepin inhibits lipopolysaccharide-induced cell migration and invasion in human colorectal carcinoma HCT-116 cells through down-regulation of prostaglandin E2 receptor EP4
Jin-Woo Jeong1, Cheol Park2, Hee-Jae Cha3, Su Hyun Hong4,5, Shin-Hyung Park6, Gi-Young Kim7, Woo Jean Kim8, Cheol Hong Kim9, Kyoung Seob Song8,*,#, Yung Hyun Choi4,5,#
1Freshwater Bioresources Utilization Bureau, Nakdonggang National Institute of Biological Resources,
2Department of Molecular Biology, Dongeui University,
3Department of Parasitology and Genetics, Kosin University College of Medicine,
4Department of Biochemistry, Dong-Eui University College of Korean Medicine,
5Anti-Aging Research Center, Dong-Eui University,
6Department of Pathology, Dong-Eui University College of Korean Medicine,
7Department of Marine Life Sciences, Jeju National University,
8Department of Anatomy, Kosin University College of Medicine,
9Department of Pediatrics, Sungkyunkwan University Samsung Changwon Hospital
Prostaglandin E2 (PGE2), a major product of cyclooxygenase-2 (COX-2), plays an important role in the carcinogenesis of many solid tumors including colorectal cancer. Because PGE2 functions by signaling through PGE2 receptors (EPs), which regulate tumor cell growth, invasion, and migration, there is growing interest in the therapeutic potential of targeting EPs. In the present study, we investigated the role of EP4 on the effectiveness of cordycepin in inhibiting migration and invasion of HCT116 human colorectal carcinoma cells. Our data indicate that cordycepin suppressed lipopolysaccharide (LPS)-enhanced cell migration and invasion through inactivation of matrix metalloproteinase (MMP)-9 and down-regulation of COX-2 expression and PGE2 production. These events were associated with inactivation of EP4 and activation of AMP-activated protein kinase (AMPK). Moreover, the EP4 antagonist AH23848 prevented LPS-induced MMP-9 expression and cell invasion in HCT116 cells. However, the AMPK inhibitor, compound C, and knockdown of AMPK activity via siRNA attenuated the cordycepin-induced inhibition of EP4 expression. Cordycepin treatment also reduced the transcriptional activity of cAMP responsive element-binding protein (CREB). These findings provide evidence that cordycepin suppresses the migration and invasion of HCT116 cells through modulating EP4 expression and the AMPK-CREB signaling pathway. Therefore, cordycepin has the potential to be a potent anti-cancer agent in therapeutic strategies against colorectal cancer metastasis.
Abstract, Accepted Manuscript(in press) [Submitted on May 28, 2018, Accepted on September 3, 2018]
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