Isolation of cDNAs that are differentially expressed between androgen-dependent and androgen-independent prostate carcinoma cells using differential display PCR

The Prostate ◽  
1995 ◽  
Vol 26 (4) ◽  
pp. 213-224 ◽  
Author(s):  
Leen J. Blok ◽  
M. Vijay Kumar ◽  
Donald J. Tindall
Keyword(s):  
Differential Display ◽  
Prostate Carcinoma ◽  
Carcinoma Cells ◽  
Differentially Expressed ◽  
Differential Display Pcr ◽  
Androgen Independent

Identification of genes differentially expressed inMycobacterium tuberculosisby differential display PCR

1998 ◽  
Vol 25 (6) ◽  
pp. 307-316 ◽  
Author(s):  
Carlos A. Rivera-Marrero ◽  
Mark A. Burroughs ◽  
Rupa A. Masse ◽  
Fredrik O. Vannberg ◽  
Darcy L. Leimbach ◽  
...  
Keyword(s):  
Differential Display ◽  
Differentially Expressed ◽  
Differential Display Pcr

Nevirapine restores hormone sensitivity in undifferentiated androgen-refractory prostate carcinoma cells

2006 ◽  
Vol 24 (18_suppl) ◽  
pp. 13149-13149
Author(s):  
M. Landriscina ◽  
C. Bagalà ◽  
A. Piscazzi ◽  
M. Quirino ◽  
N. Maiorano ◽  
...  
Keyword(s):  
Gene Expression ◽  
Prostate Cancer ◽  
Tumor Cells ◽  
Prostate Carcinoma ◽  
Carcinoma Cells ◽  
Cell Phenotype ◽  
Intermediate Cell ◽  
Hormone Sensitivity ◽  
Rt Inhibitors ◽  
Androgen Independent

13149 Background: The majority of prostate carcinomas are hormone-dependent tumors and androgen deprivation is the mainstay of therapy for advanced prostate cancer. However, androgen deprivation is ineffective on intermediate androgen-independent cells that are responsible for the hormone-refractory prostate cancer progression. Furthermore, other signaling pathways - i.e. EGF - can provide additional molecular mechanisms contributing to androgen-independent tumor progression. Reverse transcriptase (RT) inhibitors represent differentiating agents able to induce a reprogramming of gene expression in several human tumor cell models. Indeed, nevirapine and efavirenz, two widely used RT inhibitors, block the activity of endogenous RT, a gene highly expressed in tumor cells. Methods: We evaluated the ability of nevirapine to antagonize tumor growth and induce hormone sensitivity in androgen-independent human prostate tumor PC-3 cells either in vitro or in vivo. Results: Nevirapine induced the expression of several molecular markers of an androgen-dependent phenotype, such androgen receptor (AR), PSA and K18 and a reduced expression of K5, a marker of the intermediate-cell phenotype. Indeed, nevirapine enhanced the ability of prostate tumor cells to up-regulate AR in response to dihidrotestosterone. Moreover, the pharmacological inhibition of RT resulted in a significant reprogramming of gene expression, characterized by down-regulation of the notch family receptors, the EGFR1, the VEGF receptor KDR, the FGF family receptors, as well as the angiogenic factors VEGF and FGF1. Interestingly, this exocrine differentiated phenotype correlated with a reversible inhibition of cell proliferation and migration in response to nevirapine. Furthermore, the treatment of mice xenografts of prostate carcinoma cells with efavirenz and nevirapine resulted in the inhibition of tumor growth and in a reduced tumorigenic potential of cells. Conclusions: These findings suggest that RT inhibition is able to convert the androgen-independent intermediate-cell phenotype into an androgen-dependent exocrine luminal phenotype and support the need for clinical trials to test the ability of RT inhibitors and LH-RH analogs in androgen-independent prostate tumors. No significant financial relationships to disclose.

scholarly journals P2-purinergic receptor agonists inhibit the growth of androgen-independent prostate carcinoma cells.

1992 ◽  
Vol 89 (1) ◽  
pp. 191-196 ◽  
Author(s):  
W G Fang ◽  
F Pirnia ◽  
Y J Bang ◽  
C E Myers ◽  
J B Trepel
Keyword(s):  
Prostate Carcinoma ◽  
Purinergic Receptor ◽  
Carcinoma Cells ◽  
Receptor Agonists ◽  
Androgen Independent

Multidrug resistance in androgen-independent growing rat prostate carcinoma cells is mediated by P-glycoprotein

1997 ◽  
Vol 25 (1) ◽  
pp. 35-42 ◽  
Author(s):  
M. J. Siegsmund ◽  
C. Kreukler ◽  
A. Steidler ◽  
T. Nebe ◽  
K. -U. K�hrmann ◽  
...  
Keyword(s):  
Multidrug Resistance ◽  
Prostate Carcinoma ◽  
Carcinoma Cells ◽  
P Glycoprotein ◽  
Growing Rat ◽  
Rat Prostate ◽  
Androgen Independent
Sign in / Sign up

Export Citation Format

Share Document