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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2009-2-25
pubmed:abstractText
CXCR4/SDF-1alpha signal is essential for cell development, hematopoiesis, organogenesis, and vascularization as well as leukocyte trafficking. Many published reports have highlighted CXCR4 as a target in HIV infection and in cancer metastasis. In this study, we generated two specific monoclonal antibodies (MAbs 6H7 and 7D4) against human CXCR4 and found that they could recognize different antigen epitopes identified by 12G5, a commercially available anti-CXCR4 MAb. With the two MAbs, we detected the expression pattern of CXCR4 on T lymphocytes and human tumor cell lines by FCM (flow cytometry), as well as glioma tissues by immunohistochemical staining. The results showed widespread CXCR4 expression patterns in tumor cell lines and tissues and an inducible expression in CD4(+) T lymphocytes. Furthermore, we demonstrated that both of the MAbs have different functions on glioma cell line proliferation and migration in vitro. MAb 6H7 could synergistically enhance glioma cell line U251 cell proliferation induced by SDF-1alpha, while MAb 7D4 showed a blocking effect. Despite the difference in proliferation, both antibodies could attenuate chemotaxis of U251 cell induced by SDF-1alpha. Taken together, the two novel antibodies may be of great value to explore the mechanisms of SDF-1alpha CXCR4 signal in tumor cells metastasis.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
1557-8348
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
28
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
33-41
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
Characterization and application of two novel monoclonal antibodies against human CXCR4: cell proliferation and migration regulation for glioma cell line in vitro by CXCR4/SDF-1alpha signal.
pubmed:affiliation
Medical Biotechnology Institute, Soochow University, Suzhou 215007, China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't