Increased endostatin/collagen XVIII expression correlates with elevated VEGF level and poor prognosis in hepatocellular carcinoma

Liver is the primary source for collagen XVIII, the precursor of angiogenesis inhibitor, endostatin. However, the role of endostatin/collagen XVIII expression during liver carcinogenesis remains elusive. Therefore, we studied its expression in five hepatoma cell lines and 105 hepatocellular carcinom...

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Veröffentlicht in:Modern pathology 2005-05, Vol.18 (5), p.663-672
Hauptverfasser: Hu, Tsung-Hui, Huang, Chao-Cheng, Wu, Chia-Ling, Lin, Pey-Ru, Liu, Shang-Yun, Lin, Jui-Wei, Chuang, Jiin-Haur, Tai, Ming Hong
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container_title Modern pathology
container_volume 18
creator Hu, Tsung-Hui
Huang, Chao-Cheng
Wu, Chia-Ling
Lin, Pey-Ru
Liu, Shang-Yun
Lin, Jui-Wei
Chuang, Jiin-Haur
Tai, Ming Hong
description Liver is the primary source for collagen XVIII, the precursor of angiogenesis inhibitor, endostatin. However, the role of endostatin/collagen XVIII expression during liver carcinogenesis remains elusive. Therefore, we studied its expression in five hepatoma cell lines and 105 hepatocellular carcinoma specimens. The poorly differentiated hepatoma cell lines exhibited increased endostatin/collagen XVIII levels compared with the well-differentiated ones. In hepatoma tissues, endostatin/collagen XVIII expression was detected in various types of liver cells and was significantly stronger in adjacent nontumor tissues than that in tumors (P0.05). Kaplan–Meier analysis showed that patients with higher endostatin/collagen XVIII expression had significantly shorter overall survival (P=0.011) and disease-free survival (P=0.0034). Moreover, endostatin/collagen XVIII level was an independent prognostic factor for tumor recurrence (P=0.034) by multivariate analysis. In conclusion, increased endostatin/collagen XVIII expression correlated with hepatoma progression and predicted poor prognosis for patients with hepatocellular carcinoma.
doi_str_mv 10.1038/modpathol.3800336
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However, the role of endostatin/collagen XVIII expression during liver carcinogenesis remains elusive. Therefore, we studied its expression in five hepatoma cell lines and 105 hepatocellular carcinoma specimens. The poorly differentiated hepatoma cell lines exhibited increased endostatin/collagen XVIII levels compared with the well-differentiated ones. In hepatoma tissues, endostatin/collagen XVIII expression was detected in various types of liver cells and was significantly stronger in adjacent nontumor tissues than that in tumors (P&lt;0.001). Endostatin/collagen XVIII expression in nontumor tissues correlated with tumor stages (P=0.014) and expression of vascular endothelial growth factor (P=0.007), but not the stages of hepatic fibrosis (P&gt;0.05). Kaplan–Meier analysis showed that patients with higher endostatin/collagen XVIII expression had significantly shorter overall survival (P=0.011) and disease-free survival (P=0.0034). 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subjects Adult
Aged
Carcinoma, Hepatocellular - genetics
Carcinoma, Hepatocellular - metabolism
Carcinoma, Hepatocellular - pathology
Cell Line, Tumor
Collagen Type XVIII - genetics
Collagen Type XVIII - metabolism
collagen XVIII
endostatin
Endostatins - genetics
Endostatins - metabolism
Female
Gene Expression Profiling
Gene Expression Regulation, Neoplastic
HeLa Cells
hepatocellular carcinoma
Humans
Immunohistochemistry
Laboratory Medicine
Liver Neoplasms - genetics
Liver Neoplasms - metabolism
Liver Neoplasms - pathology
Male
Medicine
Medicine & Public Health
Middle Aged
Multivariate Analysis
Neoplasm Recurrence, Local
Neoplasm Staging
original-article
Pathology
Prognosis
Reverse Transcriptase Polymerase Chain Reaction - methods
RNA, Neoplasm - genetics
RNA, Neoplasm - metabolism
Survival Analysis
Vascular Endothelial Growth Factor A - metabolism
VEGF
title Increased endostatin/collagen XVIII expression correlates with elevated VEGF level and poor prognosis in hepatocellular carcinoma
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