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Prostate-specific Genes (prostate-specific + gene)

Distribution by Scientific Domains

Medical Sciences	75%

Selected Abstracts

Prostate-Specific genes and their regulation by dihydrotestosterone

THE PROSTATE, Issue 3 2008
Ma Ci
Abstract BACKGROUND Prostate is a well-known androgen-dependent tissue. METHODS By sequencing 4,294,186 serial analysis of gene expression (SAGE) tags, we have investigated the transcriptomes of normal mouse prostate, liver, testis, lung, brain, femur, skin, adipose tissue, skeletal muscle, vagina, ovary, mammary gland, and uterus in order to identify the most abundant and tissue-specific transcripts in the prostate, as well as to target the androgen responsive transcripts specifically regulated in the prostate. Small interference RNA (siRNA) in LNCaP cells was applied to validate the roles of prostate-specific/enriched ARGs in the growth of human prostate cancer cells. RESULTS The most abundant transcripts were involved in prostatic secretion, energy metabolism and immunity. Previously well-known prostate-specific transcripts, including many transcripts involved in prostatic secretion, polyamine biosynthesis and transport, and immunity were specific/enriched in the prostate. Only 22 transcripts among 114 androgen-regulated genes (ARGs) in the mouse prostate were modulated by dihydrotestosterone (DHT) in two or more tissues. The siRNA results showed that inhibition of HSPA5 and MAT2A gene expression repressed growth of human cancer LNCaP cells. Conclusions The current study globally assessed the transcriptome of the prostate and revealed the most abundant and tissue-specific transcripts which are responsible for the unique functions of this organ. These prostate-specific ARGs might be used as targets to develop safe and effective gene-based therapy for the prevention and treatment of prostate cancer. Prostate 68: 241,254, 2008. © 2007 Wiley-Liss, Inc. [source]

Erratum: Prostate-specific genes and their regulation by dihydrotestosterone.

THE PROSTATE, Issue 12 2008
André B, Fernand L, Jonny St-Amand. 2008., Lin G, Mayumi Y, Pascal B, Yasukazu T
No abstract is available for this article. [source]

RUNX1 (AML-1) and RUNX2 (AML-3) cooperate with prostate-derived Ets factor to activate transcription from the PSA upstream regulatory region

JOURNAL OF CELLULAR BIOCHEMISTRY, Issue 1 2006
Marcie Fowler
Abstract The RUNX transcription factors (RUNX1, RUNX2, and RUNX3) play essential roles in hematopoiesis and skeletal development. Consistent with these roles in differentiation and cell cycle, the activity of both RUNX1 and RUNX3 is perturbed in cancer. To determine a role for the RUNX factors in prostate biology, we investigated the expression of RUNX factors in prostate epithelial cell lines and normal prostate tissue. RUNX1, RUNX2, and RUNX3 were expressed in both normal prostate tissue and an immortalized, non-transformed cell line. We found that prostate cancer-derived cell lines expressed RUNX1 and RUNX2, but not RUNX3. Next, we sought to identify prostate-specific genes whose expression could be regulated by RUNX proteins. Four consensus RUNX sites are located within the prostate-specific antigen (PSA) regulatory region. Chromatin immunoprecipitation (ChIP) analysis showed that RUNX1 is specifically bound to the PSA regulatory region in LNCaP cells. RUNX1 and RUNX2 activated the PSA regulatory region alone or cooperatively with prostate- derived ETS factor (PDEF) and RUNX1 physically associated with PDEF. Taken together, our results suggest that RUNX factors participate in prostate epithelial cell function and cooperate with an Ets transcription factor to regulate PSA gene expression. J. Cell. Biochem. © 2005 Wiley-Liss, Inc. [source]

Gene expression changes following androgen receptor elimination in LNCaP prostate cancer cells

MOLECULAR CARCINOGENESIS, Issue 4 2003
Iris E. Eder
Abstract We have shown recently that inhibition of androgen receptor (AR) expression with an antisense AR oligonucleotide (ODN) inhibits LNCaP prostate tumor cells in vitro as well as in vivo. In this study, we investigated gene expression changes that occur after AR signaling blockade, either through AR elimination by antisense treatment or through complete androgen receptor inhibition by androgen deprivation combined with the antiandrogen bicalutamide, in order to search for genes that are directly or indirectly regulated through the AR. Gene expression changes were investigated with cDNA NIH 10K gene microarrays in response to treatment over 48 h. Expression of selected genes was further analyzed by real-time reverse transcriptase (RT)-polymerase chain reaction (PCR), Western blotting, and radioimmunoassay. A comparison of antisense-treated and androgen-deprived cells revealed several concordances such as significant downregulation of prostate-specific genes, cell-cycle regulatory genes, genes of the cholesterol biosynthesis pathway, and several cytoskeletal genes. However, there were also several genes that were differentially regulated. Among the genes that were exclusively changed by treatment with the antisense AR ODN were the insulin-like growth factor binding protein 2 (IGFBP2) and the phosphatidylinositol-4-phosphate 5-kinase type I alpha (PIP5KIA). On the other hand, complete androgen receptor blockade induced changes in the expression of the prostate overexpressed gene 1 and the S100 calcium binding protein P. In summary, we identified a cohort of interesting genes whose expression was highly affected by elimination of the AR in LNCaP prostate cancer cells. Further investigations are warranted to clarify their role in the AR signaling pathway and their susceptibility as a target for the treatment of prostate cancer. © 2003 Wiley-Liss, Inc. [source]