Role of 15-hydroxyprostaglandin dehydrogenase down-regulation on the prognosis of hepatocellular carcinoma.
- Author:
Jee Eun YANG
1
;
Eunji PARK
;
Hyo Jeong LEE
;
Hyo Jeong KANG
;
Kang Mo KIM
;
Eunsil YU
;
Danbi LEE
;
Ju Hyun SHIM
;
Young Suk LIM
;
Han Chu LEE
;
Young Hwa CHUNG
;
Yung Sang LEE
Author Information
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords: Hepatocellular carcinoma; 15-hydroxyprostaglandin dehydrogenase; Transfection; Immunohistochemistry; Survival analysis
- MeSH: Adolescent; Adult; Aged; Carcinoma, Hepatocellular/*diagnosis/mortality/pathology; Down-Regulation; Female; Hep G2 Cells; Humans; Hydroxyprostaglandin Dehydrogenases/*metabolism; Immunohistochemistry; Kaplan-Meier Estimate; Liver Neoplasms/*diagnosis/mortality/pathology; Male; Middle Aged; Prognosis; Young Adult
- From:Clinical and Molecular Hepatology 2014;20(1):28-37
- CountryRepublic of Korea
- Language:English
- Abstract: BACKGROUND/AIMS: The role of prostaglandin E2 (PGE2) in the modulation of cell growth is well established in colorectal cancer. The aim of this study was to elucidate the significance of 15-hydroxyprostaglandin dehydrogenase (15-PGDH) down-regulation on the prognosis of hepatocellular carcinoma (HCC) patients. METHODS: The expression of 15-PGDH in HCC cell lines and resected HCC tissues was investigated, and the correlation between 15-PGDH expression and HCC cell-line proliferation and patient survival was explored. RESULTS: The interleukin-1-beta-induced suppression of 15-PGDH did not change the proliferation of PLC and Huh-7 cells in the MTS [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] assay. The induction of 15-PGDH by transfection in HepG2 cells without baseline 15-PGDH expression was suppressed at day 2 of proliferation compared with empty-vector transfection, but there was no difference at day 3. Among the 153 patients who received curative HCC resection between 2003 and 2004 at our institution, 15-PGDH expression was observed in resected HCC tissues in 56 (36.6%), but the 5-year survival rate did not differ from that of the remaining 97 non-15-PGDH-expressing patients (57.1% vs 59.8%; P=0.93). Among 50 patients who exhibited baseline 15-PGDH expression in adjacent nontumor liver tissues, 28 (56%) exhibited a reduction in 15-PGDH expression score in HCC tissues, and there was a trend toward fewer long-term survivors compared with the remaining 22 with the same or increment in their 15-PGDH expression score in HCC tissues. CONCLUSIONS: The prognostic significance of 15-PGDH down-regulation in HCC was not established in this study. However, maintenance of 15-PGDH expression could be a potential therapeutic target for a subgroup of HCC patients with baseline 15-PGDH expression in adjacent nontumor liver tissue.
