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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2011-5-30
pubmed:abstractText
Vascular endothelial growth factor C (VEGF-C) is a key regulator of angiogenesis and lymphangiogenesis. VEGF-C is also implicated in the development of esophageal cancer. We investigated the mRNA levels of VEGF-C and its receptors in 38 esophageal squamous cell carcinoma specimens (ESCCs) and matched adjacent normal esophageal tissues via real-time PCR. The mRNA levels of VEGF-C, VEGFR-2 and VEGFR-3 were significantly upregulated in ESCCs versus respective side normal tissues. To explore the influence of VEGF-C on esophageal cancer progression, the expression of VEGF-C was manipulated in esophageal cancer cell lines TE-1 and Eca-109. VEGF-C transcription, translation and secretion were significantly enhanced in cells stably transfected with a VEGF-C overexpression vector or attenuated in VEGF-C shRNA-transfected cell lines. In vitro, TE-1 cells stably transfected with a VEGF-C overexpression vector exhibited an increased rate of cell proliferation, migration and focus formation, whereas knockdown of VEGF-C inhibited cell proliferation, migration and focus formation. Similar results were obtained for Eca-109 cells. VEGF-C mediated biological function through transcription of CNTN-1, which is implicated in tumor invasion and metastasis. The expression of VEGF-C was correlated with that of CNTN-1 and cell proliferation and migration induced by VEGF-C were reversed by silencing of CNTN-1. In addition, nude mice inoculated with VEGF-C shRNA-transfected cells exhibited a significantly decreased tumor size in vivo via reduced VEGFR-2 and VEGFR-3 phosphorylation and microvessel formation. VEGF-C upregulation may be involved in esophageal tumor progression. Vector-based RNA interference (RNAi) targeting VEGF-C is a potential therapeutic method for human esophageal carcinoma.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
1096-0023
pubmed:author
pubmed:copyrightInfo
Copyright © 2011 Elsevier Ltd. All rights reserved.
pubmed:issnType
Electronic
pubmed:volume
55
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
8-17
pubmed:meshHeading
pubmed-meshheading:21482472-Aged, pubmed-meshheading:21482472-Animals, pubmed-meshheading:21482472-CCAAT-Enhancer-Binding Proteins, pubmed-meshheading:21482472-Cell Line, Tumor, pubmed-meshheading:21482472-Cell Movement, pubmed-meshheading:21482472-Cell Proliferation, pubmed-meshheading:21482472-Contactin 1, pubmed-meshheading:21482472-Down-Regulation, pubmed-meshheading:21482472-Drug Resistance, Neoplasm, pubmed-meshheading:21482472-Esophageal Neoplasms, pubmed-meshheading:21482472-Female, pubmed-meshheading:21482472-Gene Expression Regulation, Neoplastic, pubmed-meshheading:21482472-Gene Knockdown Techniques, pubmed-meshheading:21482472-Gene Silencing, pubmed-meshheading:21482472-Humans, pubmed-meshheading:21482472-Male, pubmed-meshheading:21482472-Mice, pubmed-meshheading:21482472-Microvessels, pubmed-meshheading:21482472-Middle Aged, pubmed-meshheading:21482472-Precancerous Conditions, pubmed-meshheading:21482472-Promoter Regions, Genetic, pubmed-meshheading:21482472-Protein Binding, pubmed-meshheading:21482472-Vascular Endothelial Growth Factor C, pubmed-meshheading:21482472-Vascular Endothelial Growth Factor Receptor-2, pubmed-meshheading:21482472-Vascular Endothelial Growth Factor Receptor-3, pubmed-meshheading:21482472-Xenograft Model Antitumor Assays
pubmed:year
2011
pubmed:articleTitle
VEGF-C promotes the development of esophageal cancer via regulating CNTN-1 expression.
pubmed:affiliation
Department of Gastroenterology, The Affiliated Jiangyin Hospital of Southeast University, Jiangyin 214400, China. jylpf@163.com
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't