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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
1
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pubmed:dateCreated |
2000-2-9
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pubmed:abstractText |
Continuous expression of the MGSA/GROalpha, beta, or gamma chemokine bestows tumor-forming capacity to the immortalized murine melanocyte cell line, melan-a. The mechanism for this transformation is unclear, although both autocrine and paracrine processes are possible because melan-a cells as well as endothelial cells express a low level of the receptor for this ligand. To further define the role of MGSA/GRO proteins in melanocyte transformation, two types of experiments were designed to neutralize the biological effects of MGSA/GRO in the transfected melan-a clones: (1) the effect of neutralizing antiserum to MGSA/GRO proteins on melan-a tumor growth was assessed; (2) the tumor-forming capacity of melan-a clones expressing ELR motif-mutated forms of MGSA/GRO with compromised receptor affinity was compared to the tumor-forming capacity of clones expressing wild-type MGSA/GRO. These experiments revealed that SCID mice inoculated with MGSA/GROalpha- or gamma-expressing melan-a cells and subsequently treated with antiserum to the respective chemokine exhibited decreased tumor growth. This reduction in tumor growth was accompanied by declining angiogenic activity in MGSA/GROgamma-expressing tumors. Moreover, athymic nude mice injected with melan-a cells expressing ELR-mutant forms of MGSA/GROalpha exhibited markedly impaired tumor-forming capacity compared with those mice injected with melan-a clones expressing wild-type MGSA/GRO. These data suggest that continuous expression of MGSA/GRO proteins may facilitate tumor growth by stimulating the growth of microvessels into the tumor (paracrine) and by affecting melanocyte growth (autocrine).
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/10647998-10221914,
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
0741-5400
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
67
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
53-62
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pubmed:dateRevised |
2011-5-5
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pubmed:meshHeading |
pubmed-meshheading:10647998-Animals,
pubmed-meshheading:10647998-Cell Transformation, Neoplastic,
pubmed-meshheading:10647998-Chemokine CXCL1,
pubmed-meshheading:10647998-Chemokines, CXC,
pubmed-meshheading:10647998-Chemotactic Factors,
pubmed-meshheading:10647998-Female,
pubmed-meshheading:10647998-Gene Expression Regulation, Neoplastic,
pubmed-meshheading:10647998-Growth Substances,
pubmed-meshheading:10647998-Intercellular Signaling Peptides and Proteins,
pubmed-meshheading:10647998-Melanoma, Experimental,
pubmed-meshheading:10647998-Mice,
pubmed-meshheading:10647998-Mice, Nude,
pubmed-meshheading:10647998-Neoplasm Proteins,
pubmed-meshheading:10647998-Neovascularization, Pathologic
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pubmed:year |
2000
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pubmed:articleTitle |
The tumorigenic and angiogenic effects of MGSA/GRO proteins in melanoma.
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pubmed:affiliation |
Department of Cell Biology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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