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Background: Abnormal upregulation of prostaglandin E2 (PGE2) is considered to be a key oncogenic event in the development and progression of inflammation-associated human colon cancer. It has been reported that 15-hydroxyprostaglandin dehydrogenase (15-PGDH), an enzyme catabolizing PGE2, is ubiquitously downregulated in human colon cancer. 15-Deoxy-12,14-prostaglandin J2 (15d-PGJ2), a peroxisome proliferator-activated receptor ligand, has been shown to have anticarcinogenic activities. In this study, we investigate the effect of 15d-PGJ2 on expression of 15-PGDH in human colon cancer HCT116 cells. Methods: HCT116 cells were treated with 15d-PGJ2 analysis. The expression of 15-PGDH in the treated cells was measured by Western blot analysis and RT-PCR. In addition, the cells were subjected to a 15-PGDH activity assay. To determine which transcription factor(s) and signaling pathway(s) are involved in 15d-PGJ2-induced 15-PGDH expression, we performed a cDNA microarray analysis of 15d-PGJ2-treated cells. The DNA binding activity of AP-1 was measured by an electrophoretic mobility shift assay. To determine whether the AP-1 plays an important role in the 15d-PGJ2-induced 15-PGDH expression, the cells were transfected with siRNA of c-Jun, a major subunit of AP-1. To elucidate the upstream signaling pathways involved in AP-1 activation by 15d-PGJ2, we examined its effect on phosphorylation of Akt by Western blot analysis in the presence or absence of kinase inhibitor. Results: 15d-PGJ2 (10 M) significantly upregulated 15-PGDH expression at the mRNA and protein levels in HCT-116 cells. 15-PGDH activity was also elevated by 15d-PGJ2. We observed that genes encoding C/EBP delta, FOS-like antigen 1, c-Jun, and heme oxygenase-1 (HO-1) were most highly induced in the HCT116 cells following 15d-PGJ2 treatment. 15d-PGJ2 increased the DNA binding activity of AP-1. Moreover, transfection with specific siRNA against c-Jun significantly reduced 15-PGDH expression induced by 15d-PGJ2. 15d-PGJ2 activates Akt and a pharmacological inhibitor of Akt, LY294002, abrogated 15d-PGJ2-induced 15-PGDH expression. We also observed that an inhibitor of HO-1, zinc protoporphyrin IX, also abrogated upregulation of 15-PGDH and down-regulation of cyclooxygenase-2 expression induced by 15d-PGJ2. Conclusions: These finding suggest that 15d-PGJ2 upregulates the expression of 15-PGDH through AP-1 activation in colon cancer HCT116 cells. (J Cancer Prev 2019;24:183-191)
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참고문헌 (31)
참고문헌 신청
Karpisheh V / 2019 / Prostaglandin E2 as a potent therapeutic target for treatment of colon cancer / Prostaglandins Other Lipid Mediat 144:106338
Greenhough A / 2009 / The COX-2/PGE2 pathway: key roles in the hallmarks of cancer and adaptation to the tumour microenvironment / Carcinogenesis 30:377~386
Tai HH / 2006 / NAD+-linked 15-hydroxyprostaglandin dehydrogenase: structure and biological functions / Curr Pharm Des 12:955~962
Kim HB / 2017 / Prostaglandin E2 activates YAP and a positive-signaling loop to promote colon regeneration after colitis but also carcinogenesis in mice / Gastroenterology 152:616~630
Myung SJ / 2006 / 15-Hydroxyprostaglandin dehydrogenase is an in vivo suppressor of colon tumorigenesis / Proc Natl Acad Sci USA 103:12098~12102
Greenhough A / 2009 / The COX-2/PGE2 pathway: key roles in the hallmarks of cancer and adaptation to the tumour microenvironment / Carcinogenesis 30:377~386
Tai HH / 2006 / NAD+-linked 15-hydroxyprostaglandin dehydrogenase: structure and biological functions / Curr Pharm Des 12:955~962
Kim HB / 2017 / Prostaglandin E2 activates YAP and a positive-signaling loop to promote colon regeneration after colitis but also carcinogenesis in mice / Gastroenterology 152:616~630
Myung SJ / 2006 / 15-Hydroxyprostaglandin dehydrogenase is an in vivo suppressor of colon tumorigenesis / Proc Natl Acad Sci USA 103:12098~12102
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