Regulation of the expression of protein kinase C isoenzymes in rat ventral prostate: effects of age, castration and flutamide treatment

Montalvo, Leire; Sánchez‐Chapado, Manuel; Prieto, Juan Carlos; Carmena, Marı́a J.

doi:10.1016/s0024-3205(02)02016-7

Cited by 11 publications

(9 citation statements)

References 30 publications

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“…Results are representative of six independent experiments. Scale bar is 10 mm that is induced by either surgical castration or androgendeprivation therapy (Montalvo et al, 2002). These observations, together with the data presented here, indicated that the ability of PKCe to block certain forms of Bax-mediated apoptosis may not be sufficient to ensure the survival of CaP cells throughout the involution-regeneration cycle that is characteristic of recurrent CaP.…”

Section: Survival Of Pkce-positive Epithelial Cells During the Progrementioning

confidence: 72%

Protein kinase Cɛ interacts with Bax and promotes survival of human prostate cancer cells

et al. 2003

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Section: Survival Of Pkce-positive Epithelial Cells During the Progrementioning

confidence: 72%

Protein kinase Cɛ interacts with Bax and promotes survival of human prostate cancer cells

et al. 2003

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“…The PKC family is interesting as various important PKC isoforms have been shown to be androgenregulated in the rat ventral prostate (Montalvo et al 2002). Inhibitor treatment also altered the expression of several ras/rab-related genes in a segment-specific way.…”

Section: Discussionmentioning

confidence: 99%

Effects of PNU157706, a dual 5alpha-reductase inhibitor, on gene expression in the rat epididymis

Henderson¹,

Cooke²,

Robaire³

2004

Journal of Endocrinology

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The epididymis is the site of sperm maturation and storage. 5 -Reductases (types 1 and 2) are key enzymes in this tissue because they convert testosterone to dihydrotestosterone (DHT), the main androgen regulating epididymal functions. Examining the consequences of inhibiting DHT formation is likely to provide important information regarding the regulation of epididymal functions, yet few inhibitor studies have focused on this tissue. To understand better DHT-mediated regulation of epididymal gene expression, we employed a dual 5 -reductase inhibitor and cDNA microarrays to examine the effects of 5 -reductase inhibition on gene expression in the initial segment, caput, corpus, and cauda epididymidis. Inhibition of epididymal 5 -reductase activity by PNU157706 was confirmed by in vitro enzyme assays. Rats were treated with 0, 0·1, 1·0 or 10 mg/kg per day PNU157706 for 28 days. The weights of DHT-dependent tissues, including the epididymis, were decreased following treatment. The effect of treatment on gene expression was dose-dependent and highly segment-specific. The initial segment responded uniquely in that a similar number of genes increased and decreased in expression compared with the other segments where the majority of affected genes decreased in expression. Some of the more dramatically affected genes were involved in signal transduction as well as fatty acid and lipid metabolism, regulation of ion and fluid transport, luminal acidification, oxidative defense and protein processing and degradation. These are essential processes contributing to the formation of an optimal luminal microenvironment required for proper sperm maturation. These results provide a novel insight into the DHT-dependent mechanisms that control epididymal functions.

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“…Differences related to cell batch or to the antibody used may underpin our ability to detect PKCb1 expression in LNCaP cells. Moreover, we have recently observed the same pattern of expression of PKCb1 in rat prostate [21], which has been shown to express PKCb1 mRNA [26].…”

Section: Discussionmentioning

confidence: 80%

“…We have previously observed that flutamide increases the expression of ventral prostate PKC isoenzymes (a, b, f and e) from both control and castrated rats [21]. In this study we analyzed the effect of flutamide on the level of expression of these four PKC isoenzymes in LNCaP and PC3 human prostate cancer cells.…”

Section: Resultsmentioning

confidence: 96%

“…We have previously shown that treatment of rats with flutamide blocks adenylate cyclase activation through G-protein coupled receptors in prostate cell membranes [19], a pattern that is also evoked by PKC activation in rat prostate cells [20]. Moreover, we have recently observed that flutamide upregulates the expression of different PKC isoenzymes in both normal and castrated rat prostates [21]. In the present report, we address the study of the regulation of the expression of four (a, b1, e, f) PKC isoforms in prostate cancer cells by flutamide and by androgen availability.…”

Section: Introductionmentioning

confidence: 95%

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Effects of the Antiandrogen Flutamide on the Expression of Protein Kinase C Isoenzymes in LNCaP and PC3 Human Prostate Cancer Cells

et al. 2004

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Flutamide is a nonsteroidal antiandrogen that is frequently used for total androgen blockage in the treatment of advanced prostate cancer. We investigated the effect of this antiandrogen on the expression of protein kinase C (PKC) isoenzymes (a, b1, e, f) that are involved in cell growth, apoptosis and neoplastic transformation. Androgen-dependent (LNCaP) and independent (PC3) human prostate cancer cells were cultured in a medium that contained fetal bovine serum (FBS) or charcoal-stripped serum (CSS) and treated with 10 lM flutamide. The expression of PKC isoenzymes and the androgen receptor (AR) were analyzed by Western blot and RT-PCR, respectively. Serum steroids differentially regulate the expression of PKC isoenzymes in LNCaP and PC3 cells. Flutamide up-regulated the expression of a, b1 and f, but not e, PKC isoenzymes in CSS-LNCaP cells. These results were not homogeneously reproduced in the presence of androgens. We observed an opposite effect of flutamide, compared to CSS, on PKCb1 isoform expression in CSS-LNCaP suggesting that this antiandrogen exerts an agonistic effect. In PC3 cells flutamide potentiated the expression of the four PKC isoenzymes in almost all conditions tested (FBS-and CSScultured cells). Such effect of flutamide in PC3 cells is independent of AR since no expression of AR was detected. These results provide new evidence on antagonistic/agonistic responses of prostate cancer cells to antiandrogen drugs that are widely used in therapy and show that flutamide can elicit responses in prostate cancer cells that do not express AR.

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Regulation of the expression of protein kinase C isoenzymes in rat ventral prostate: effects of age, castration and flutamide treatment

Cited by 11 publications

References 30 publications

Protein kinase Cɛ interacts with Bax and promotes survival of human prostate cancer cells

Protein kinase Cɛ interacts with Bax and promotes survival of human prostate cancer cells

Effects of PNU157706, a dual 5alpha-reductase inhibitor, on gene expression in the rat epididymis

Effects of the Antiandrogen Flutamide on the Expression of Protein Kinase C Isoenzymes in LNCaP and PC3 Human Prostate Cancer Cells

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