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rdf:type |
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lifeskim:mentions |
umls-concept:C0006675,
umls-concept:C0007634,
umls-concept:C0010592,
umls-concept:C0017262,
umls-concept:C0017636,
umls-concept:C0021469,
umls-concept:C0035647,
umls-concept:C0079633,
umls-concept:C0086418,
umls-concept:C0185117,
umls-concept:C0205281,
umls-concept:C1280500,
umls-concept:C2911684
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pubmed:issue |
41
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pubmed:dateCreated |
2004-9-16
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pubmed:abstractText |
Interleukin (IL)-8 produced from glioblastoma is suggested to contribute to its own proliferation and progression. Since various external stimuli have been shown to increase intracellular Ca(2+) in glioma cells, we investigated Ca(2+) mobilization-dependent IL-8 expression and effect of cyclosporin A (CsA), an inhibitor of calcineurin (Cn), on the expression and invasive potential of human glioblastoma U251MG cells. Combined treatment with Ca(2+)-ionophore and phorbol-myristate-acetate (A23187/PMA) increased IL-8 mRNA and protein levels. This increase was suppressed by CsA and by another Cn inhibitor FK506. Luciferase reporter gene assay and electrophoretic mobility shift assay revealed that activation of p65-containing nuclear factor-kappaB was essential for A23187/PMA-dependent activation of IL-8 promoter. CsA suppressed the promoter activity by attenuating IkappaB-alpha degradation. U251MG cells expressed IL-8 receptors CXCR-1 and -2, and Matrigel invasion assay revealed that CsA attenuated A23187/PMA-dependent stimulation of invasive potential, probably by inhibiting IL-8 production. In addition, IL-8-dependent proliferation was also suppressed by CsA. Taken together, these results demonstrate the novel inhibitory effects of CsA on glioblastoma cell functions, suggesting CsA as a potential therapeutic adjuvant for glioma treatment.
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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 |
http://linkedlifedata.com/resource/pubmed/chemical/CHUK protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Calcimycin,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclosporine,
http://linkedlifedata.com/resource/pubmed/chemical/I-kappa B Kinase,
http://linkedlifedata.com/resource/pubmed/chemical/IKBKB protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/IKBKE protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-8,
http://linkedlifedata.com/resource/pubmed/chemical/NF-kappa B,
http://linkedlifedata.com/resource/pubmed/chemical/Protein-Serine-Threonine Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interleukin-8A,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interleukin-8B,
http://linkedlifedata.com/resource/pubmed/chemical/Tetradecanoylphorbol Acetate
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
0950-9232
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
9
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pubmed:volume |
23
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
6924-32
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:15286717-Calcimycin,
pubmed-meshheading:15286717-Calcium,
pubmed-meshheading:15286717-Cell Division,
pubmed-meshheading:15286717-Cell Line, Tumor,
pubmed-meshheading:15286717-Cyclosporine,
pubmed-meshheading:15286717-Glioblastoma,
pubmed-meshheading:15286717-Humans,
pubmed-meshheading:15286717-I-kappa B Kinase,
pubmed-meshheading:15286717-Interleukin-8,
pubmed-meshheading:15286717-NF-kappa B,
pubmed-meshheading:15286717-Neoplasm Invasiveness,
pubmed-meshheading:15286717-Promoter Regions, Genetic,
pubmed-meshheading:15286717-Protein-Serine-Threonine Kinases,
pubmed-meshheading:15286717-RNA, Messenger,
pubmed-meshheading:15286717-Receptors, Interleukin-8A,
pubmed-meshheading:15286717-Receptors, Interleukin-8B,
pubmed-meshheading:15286717-Tetradecanoylphorbol Acetate
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pubmed:year |
2004
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pubmed:articleTitle |
Inhibitory effects of cyclosporin A on calcium mobilization-dependent interleukin-8 expression and invasive potential of human glioblastoma U251MG cells.
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pubmed:affiliation |
Department of Endocrinology and Metabolism, Division of Molecular and Cellular Adaptation, Research Institute of Environmental Medicine, Nagoya University, Furo-cho, Chikusa-ku, Nagoya 464-8601, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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