Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2011-3-1
pubmed:abstractText
Epithelial neutrophil-activating peptide-78 (CXCL5), a member of the CXC chemokine family, has been shown to be involved in angiogenesis, tumor growth, and metastasis. The objective of this study was to determine the relationship between CXCL5 expression and tumor progression in human pancreatic cancer and to elucidate the mechanism underlying CXCL5-mediated tumor angiogenesis and cancer growth. We report herein that CXCL5 is overexpressed in human pancreatic cancer compared with paired normal pancreas tissue. Overexpression of CXCL5 is significantly correlated with poorer tumor differentiation, advanced clinical stage, and shorter patient survival. Patients with pancreatic cancer and CXCL5 overexpression who underwent resection of cancer had a mean survival time 25.5 months shorter than that of patients who did not overexpress CXCL5. Blockade of CXCL5 or its receptor CXCR2 by small-interfering RNA knockdown or antibody neutralization attenuated human pancreatic cancer growth in a nude mouse model. Finally, we demonstrated that CXCL5 mediates pancreatic cancer-derived angiogenesis through activation of several signaling pathways, including protein kinase B (Akt), extracellular signal-regulated kinase (ERK), and signal transducer and activator of transcription (STAT) in human endothelial cells. These data suggest that CXCL5 is an important mediator of tumor-derived angiogenesis and that it may serve as a survival factor for pancreatic cancer. Blockade of either CXCL5 or CXCR2 may be a critical adjunct antiangiogenic therapy against pancreatic cancer.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
1525-2191
pubmed:author
pubmed:copyrightInfo
Copyright © 2011 American Society for Investigative Pathology. Published by Elsevier Inc. All rights reserved.
pubmed:issnType
Electronic
pubmed:volume
178
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1340-9
pubmed:dateRevised
2011-9-26
pubmed:meshHeading
pubmed-meshheading:21356384-Animals, pubmed-meshheading:21356384-Cell Line, Tumor, pubmed-meshheading:21356384-Cell Proliferation, pubmed-meshheading:21356384-Chemokine CXCL5, pubmed-meshheading:21356384-Disease Progression, pubmed-meshheading:21356384-Endothelial Cells, pubmed-meshheading:21356384-Extracellular Signal-Regulated MAP Kinases, pubmed-meshheading:21356384-Gene Expression Regulation, Neoplastic, pubmed-meshheading:21356384-Gene Knockdown Techniques, pubmed-meshheading:21356384-Humans, pubmed-meshheading:21356384-Mice, pubmed-meshheading:21356384-Mice, Nude, pubmed-meshheading:21356384-Neovascularization, Pathologic, pubmed-meshheading:21356384-Neutralization Tests, pubmed-meshheading:21356384-Pancreatic Neoplasms, pubmed-meshheading:21356384-Phosphorylation, pubmed-meshheading:21356384-Proto-Oncogene Proteins c-akt, pubmed-meshheading:21356384-RNA, Messenger, pubmed-meshheading:21356384-Receptors, Interleukin-8B, pubmed-meshheading:21356384-Survival Analysis, pubmed-meshheading:21356384-Xenograft Model Antitumor Assays
pubmed:year
2011
pubmed:articleTitle
Overexpression of CXCL5 is associated with poor survival in patients with pancreatic cancer.
pubmed:affiliation
Department of Surgery, Hirshberg Laboratories for Pancreatic Cancer Research, David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, California 90095-6904, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural