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Role of 15-hydroxyprostaglandin dehydrogenase down-regulation on the prognosis of hepatocellular carcinoma.

Yang JE, Park E, Lee HJ, Kang HJ, Kim KM, Yu E, Lee D, Shim JH, Lim YS, Lee HC, Chung YH, Lee YS - Clin Mol Hepatol (2014)

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: Department of Internal Medicine, Asan Liver Center, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.

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-β-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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Related in: MedlinePlus

The induction of 15-PGDH expression in HepG2 cells by transfection with a vector encoding WT 15-PGDH. Transfection was confirmed by green fluorescent proteins taining (A) and immunoblotting for 15-PGDH (B). Huh-7 cells were used as a positive control. 15-PGDH expression was stronger at day 0 than at day 3 of transfection.
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Figure 3: The induction of 15-PGDH expression in HepG2 cells by transfection with a vector encoding WT 15-PGDH. Transfection was confirmed by green fluorescent proteins taining (A) and immunoblotting for 15-PGDH (B). Huh-7 cells were used as a positive control. 15-PGDH expression was stronger at day 0 than at day 3 of transfection.

Mentions: In HepG2 cells, which did not show baseline expression of 15-PGDH, we induced 15-PGDH expression by transfection with vector encoding WT 15-PGDH. Transfection was confirmed by GFP staining (Fig. 3A) and immunoblotting for 15-PGDH (Fig. 3B). 15-PGDH expression was strongest at day 0 of transfection and then diminished slowly as time goes by (Fig. 3B). Proliferation assay showed 15-PGDH expression induction in HepG2 cells suppressed cell growth at day 2, but this growth difference disappeared at day 3 of MTS assay (Fig. 4).


Role of 15-hydroxyprostaglandin dehydrogenase down-regulation on the prognosis of hepatocellular carcinoma.

Yang JE, Park E, Lee HJ, Kang HJ, Kim KM, Yu E, Lee D, Shim JH, Lim YS, Lee HC, Chung YH, Lee YS - Clin Mol Hepatol (2014)

The induction of 15-PGDH expression in HepG2 cells by transfection with a vector encoding WT 15-PGDH. Transfection was confirmed by green fluorescent proteins taining (A) and immunoblotting for 15-PGDH (B). Huh-7 cells were used as a positive control. 15-PGDH expression was stronger at day 0 than at day 3 of transfection.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3992327&req=5

Figure 3: The induction of 15-PGDH expression in HepG2 cells by transfection with a vector encoding WT 15-PGDH. Transfection was confirmed by green fluorescent proteins taining (A) and immunoblotting for 15-PGDH (B). Huh-7 cells were used as a positive control. 15-PGDH expression was stronger at day 0 than at day 3 of transfection.
Mentions: In HepG2 cells, which did not show baseline expression of 15-PGDH, we induced 15-PGDH expression by transfection with vector encoding WT 15-PGDH. Transfection was confirmed by GFP staining (Fig. 3A) and immunoblotting for 15-PGDH (Fig. 3B). 15-PGDH expression was strongest at day 0 of transfection and then diminished slowly as time goes by (Fig. 3B). Proliferation assay showed 15-PGDH expression induction in HepG2 cells suppressed cell growth at day 2, but this growth difference disappeared at day 3 of MTS assay (Fig. 4).

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: Department of Internal Medicine, Asan Liver Center, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.

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-β-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.

Show MeSH
Related in: MedlinePlus