Role of 15-hydroxyprostaglandin dehydrogenase down-regulation on the prognosis of hepatocellular carcinoma
Korean Journal of Hepatology 2014³â 20±Ç 1È£ p.28 ~ p.37
¾çÁöÀº(Yang Jee-Eun) - University of Ulsan College of Medicine Asan Medical Center Department of Internal Medicine
¹ÚÀºÁö(Park Eun-Ji) - University of Ulsan College of Medicine Asan Medical Center Department of Internal Medicine
ÀÌÈ¿Á¤(Lee Hyo-Jeong) - University of Ulsan College of Medicine Asan Medical Center Department of Internal Medicine
°È¿Á¤(Kang Hyo-Jeong) - University of Ulsan College of Medicine Department of Pathology
±è°¸ð(Kim Kang-Mo) - University of Ulsan College of Medicine Asan Medical Center Department of Internal Medicine
À¯Àº½Ç(Yu Eun-Sil) - University of Ulsan College of Medicine Department of Pathology
À̴ܺñ(Lee Dan-Bi) - University of Ulsan College of Medicine Asan Medical Center Department of Internal Medicine
½ÉÁÖÇö(Shim Ju-Hyun) - University of Ulsan College of Medicine Asan Medical Center Department of Internal Medicine
ÀÓ¿µ¼®(Lim Young-Suk) - University of Ulsan College of Medicine Asan Medical Center Department of Internal Medicine
ÀÌÇÑÁÖ(Lee Han-Chu) - University of Ulsan College of Medicine Asan Medical Center Department of Internal Medicine
Á¤¿µÈ(Chung Young-Hwa) - University of Ulsan College of Medicine Asan Medical Center Department of Internal Medicine
ÀÌ¿µ»ó(Lee Yung-Sang) - University of Ulsan College of Medicine Asan Medical Center Department of Internal Medicine
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-¥â-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.
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Hepatocellular carcinoma, 15-hydroxyprostaglandin dehydrogenase, Transfection, Immunohistochemistry, Survival analysis
KMID :
1103920140200010028
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