Laminin-5-mediated gene expression in human prostate carcinoma cells

Interactions between extracellular matrix (ECM) proteins and prostate carcinoma cells provide a dynamic model of prostate tumor progression. Previous work in our laboratory showed that laminin‐5, an important member of a family of ECM glycoproteins expressed in the basal lamina, is lost in prostate...

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Veröffentlicht in:Molecular carcinogenesis 2001-02, Vol.30 (2), p.119-129
Hauptverfasser: Calaluce, Robert, Kunkel, Mark W., Watts, George S., Schmelz, Monika, Hao, Junshan, Barrera, Jean, Gleason-Guzman, Mary, Isett, Robert, Fitchmun, Mark, Bowden, G. Tim, Cress, Anne E., Futscher, Bernard W., Nagle, Raymond B.
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Sprache:eng
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Zusammenfassung:Interactions between extracellular matrix (ECM) proteins and prostate carcinoma cells provide a dynamic model of prostate tumor progression. Previous work in our laboratory showed that laminin‐5, an important member of a family of ECM glycoproteins expressed in the basal lamina, is lost in prostate carcinoma. Moreover, we showed that the receptor for laminin‐5, the α6β4 integrin, is altered in prostate tumors. However, the genes that laminin‐5 potentially regulates and the significance of its loss of expression in prostate cancer are not known. We selected cDNA microarray as a comprehensive and systematic method for surveying and examining gene expression induced by laminin‐5. To establish a definitive role for laminin‐5 in prostate tumor progression and understand the significance of its loss of expression, we used a cDNA microarray containing 5289 human genes to detect perturbations of gene expression when DU145 prostate carcinoma cells interacted with purified laminin‐5 after 0.5, 6, and 24 h. Triplicate experiments showed modulations of four, 61, and 14 genes at 0.5, 6, and 24 h, respectively. Genes associated with signal transduction, cell adhesion, the cell cycle, and cell structure were identified and validated by northern blot analysis. Protein expression was further assessed by immunohistochemistry. Mol. Carcinog. 30:119–129, 2001. © 2001 Wiley‐Liss, Inc.
ISSN:0899-1987
1098-2744
DOI:10.1002/1098-2744(200102)30:2<119::AID-MC1020>3.0.CO;2-N