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Human laminin‐5 and laminin‐10 mediated gene expression of prostate carcinoma cells
Author(s) -
Calaluce Robert,
Beck Shaleen K.,
Bair Elisabeth L.,
Pandey Ritu,
Greer Kevin A.,
Hoying Adam M.,
Hoying James B.,
Mount David W.,
Nagle Raymond B.
Publication year - 2006
Publication title -
the prostate
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.295
H-Index - 123
eISSN - 1097-0045
pISSN - 0270-4137
DOI - 10.1002/pros.20393
Subject(s) - laminin , prostate , gene expression , carcinoma , gene , prostate carcinoma , cancer research , prostate cancer , medicine , biology , pathology , cancer , extracellular matrix , microbiology and biotechnology , genetics
In prostate cancer progression, the basal lamina switches from predominantly laminin‐5 to laminin‐10. DU‐145 prostate cancer cells were treated with either soluble laminin‐5 (20 ng/ml) or laminin‐10 (1 µg/ml) for 6, 24, and 48 hr. Total RNA was harvested for a 7,500 human cDNA microarray. Hybridizations were carried out in accordance with a 10 sample analysis of variance (ANOVA) statistical model. One thousand one hundred sixteen genes had measurable expression 2 standard deviations above background and 50% of spots for any given sample for all hybridizations were positive. Expression values of significantly varying genes were clustered and a list of 408 genes ( P < 0.05) with a 1.5 or greater fold change in at least one time point were chosen for further analysis. Seventy eight changed in a time‐dependent manner with laminin‐10 treatment, 85 changed with laminin‐5, and 13 showed changes with both treatments. The 408 genes that passed a paired t ‐test in at least one time‐dependent category were further analyzed using Pathway Miner. One of the largest gene association networks involved signal transduction in the growth factor‐MAP kinase pathways. EGFR was validated by real‐time PCR and laminin‐10 mediated cell adhesion activated EGFR in DU‐145 cells. Both laminins appear to be important signal transducers in prostate cancer. Prostate 66: 1381–1390, 2006. © 2006 Wiley‐Liss, Inc.