Title of article :
Differentially expressed genes in the prostate cancer cell line LNCaP after exposure to androgen and anti-androgen
Author/Authors :
Coutinho-Camillo، نويسنده , , Clلudia M. and Salaorni، نويسنده , , Sibeli and Sarkis، نويسنده , , ءlvaro S. and Nagai، نويسنده , , Maria A.، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 2006
Pages :
9
From page :
130
To page :
138
Abstract :
Androgens play an important role in growth and maintenance of prostate cells. The actions of androgens are mediated by the androgen receptor (AR), a transcription factor member of the super-family of nuclear hormone receptors. Androgen regulated genes (ARGs) are potential markers for early diagnosis and treatment of prostate cancer patients. In the present study, we used DDRT-PCR (differential display reverse transcriptase polymerase chain reaction) technique in order to investigate differentially expressed genes in the prostate cancer cell line LNCaP after treatment with dihydrotestosterone and bicalutamide for 6, 24, and 48 hours. Fifty-five differentially expressed fragments were isolated, cloned, and sequenced. Sequencing analysis of these fragments revealed 56 different transcripts that showed homology to transcription factors, cell cycle regulators, metabolic enzymes, and hypothetical proteins. Among the differentially expressed genes, SPA17 and DDEF2 were further validated using quantitative real time RT-PCR (qPCR) in a series of 25 prostate tumor samples. The DDEF2 gene is involved in adhesion and cell migration of monocytes, and the SPA17 gene might be involved in cellular signal transduction. The transcripts of both, SPA17 and DDEF2 genes, showed altered pattern of expression in the group of prostate tumors analyzed by qPCR. The differentially expressed genes identified in this study might provide new insights into the androgen signaling pathways in prostate cells.
Journal title :
Cancer Genetics and Cytogenetics
Serial Year :
2006
Journal title :
Cancer Genetics and Cytogenetics
Record number :
1827526
Link To Document :
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