Retinoid and androgen regulation of cell growth, epidermal growth factor and retinoic acid receptors in normal and carcinoma rat prostate cells

Richter, Frank; Huang, Huei-Ping; Li, Ming Tang; Danielpour, David; Wang, Shoou Lih; Irwin, R. John

doi:10.1016/s0303-7207(99)00095-7

Cited by 25 publications

(18 citation statements)

References 23 publications

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“…However, a conflicting report by Richter et al showed that NRP-154 cells express low levels of the androgen receptor by northern blotting analysis. 13 In our initial studies, we confirmed the androgen receptor status of the NRP-152 and NRP-154 cells as their androgen receptor status was central to our hypothesis.…”

Section: Discussionsupporting

confidence: 67%

Epigallocatechin‐3‐gallate and bicalutamide cause growth arrest and apoptosis in NRP‐152 and NRP‐154 prostate epithelial cells

et al. 2007

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Aim: A number of epidemiological studies have suggested that consumption of green tea reduces the risk of prostate cancer. The aim of this study was to elucidate the effects of epigallocatechin-3-gallate (EGCG), one of the major constituents of green tea, on growth inhibition and apoptosis in prostate epithelial cell lines with and without bicalutamide. Methods: The effects of EGCG and bicalutamide alone and in combination were examined on NRP-152 and NRP-154 cells derived from the dorso-lateral prostate of the Lobund-Wistar rat. Following treatments, cell number and levels of apoptosis were assessed. Results: After treatment with EGCG, both cell lines displayed a dose-dependent decrease in cell number; this effect was more pronounced in NRP-154 cells. This decrease in cell number was caused by growth arrest in NRP-152 cells and apoptosis in NRP-154 cells. The apoptotic events in the NRP-154 cells were concurrent with a loss of manganese superoxide dismutase expression. Androgen ablation was achieved by androgen withdrawal using charcoal stripped serum or treatment with bicalutamide. Bicalutamide decreased cell number and induced apoptosis in a dose-dependent manner in both cell lines; however, androgen withdrawal did not. There was a loss of androgen receptor expression in NRP-152 cells with bicalutamide treatment. However, as the NRP-154 cells are androgen receptor negative, the loss in cell number and increased apoptotic events in these cells cannot be attributed to the anti-androgenic activity of bicalutamide. Cells treated with a combination of bicalutamide and EGCG also demonstrated a dose-dependent decrease in cell number that was significantly greater than bicalutamide alone. Conclusions: This study demonstrates the potential use of EGCG and other antioxidants as therapeutic candidates for prostate cancer.

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Section: Discussionsupporting

confidence: 67%

Epigallocatechin‐3‐gallate and bicalutamide cause growth arrest and apoptosis in NRP‐152 and NRP‐154 prostate epithelial cells

et al. 2007

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“…Retinoids are required for homeostasis of mature prostate: consumption of a retinoid-deficient diet caused keratinization of prostate epithelium in adult rats (Wolbach and Howe, 1925) and keratinized prostate epithelium and squamous metaplasia in adult mice (Lohnes et al, 1993). There is also evidence that RAR activity may be linked to prostate growth, since nuclear localization of RAR␣ and RAR␥ increases during benign prostate disease and prostate cancer in humans (Gyftopoulos et al, 2000;Richter et al, 2002) and in a rat prostate cancer model (Richter et al, 1999).…”

Section: Introductionmentioning

confidence: 99%

Retinoic acid induces prostatic bud formation

Vezina

Allgeier

Fritz

et al. 2008

Developmental Dynamics

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Formation of prostatic buds from the urogenital sinus (UGS) to initiate prostate development requires localized action of several morphogenetic factors. This report reveals all-trans-retinoic acid (RA) to be a powerful inducer of mouse prostatic budding that is associated with reciprocal changes in expression of two regulators of budding: sonic hedgehog (Shh) and bone morphogenetic protein 4 (Bmp4). Localization of retinoid signaling and expression of RA synthesis, metabolism, and receptor genes in the UGS on embryonic days 14.5-17.5 implicate RA in the mechanism of bud initiation. In UGS organ culture, RA increased prostatic budding, increased Shh expression, and decreased Bmp4. Prostatic budding was stimulated in the absence of RA by recombinant SHH, by blocking BMP4 signaling with NOGGIN, or by combined treatment with SHH and NOGGIN in UGS organ culture media. These observations suggest that reciprocal changes in hedgehog and BMP signaling by RA may regulate bud initiation. Developmental Dynamics 237:1321-1333, 2008.

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“…Early experiments on mouse prostate explant cultures showed that all-trans-retinoic acid (trans-RA) could both inhibit and reverse the proliferative effects of chemical carcinogens on prostatic epithelium (Lasnitzki & Goodman 1974, Chopra & Wilkoff 1976. Recent studies have demonstrated that retinoids effectively inhibit the growth of prostate cancer cells in vitro and suppress the development of prostate carcinogenesis (Blutt et al 1997, DiPaola et al 1997, Campbell et al 1998, Goossens et al 1999, McCormick et al 1999, Pasquali et al 1999, Richter et al 1999, Sun et al 1999b, Urban et al 1999, Webber et al 1999, Kelly et al 2000, Koshiuka et al 2000, Lotan et al 2000, Tanabe 2000, Pili et al 2001. Clinical trials of several retinoids and their combination with other anti-cancer agents have shown significant activities, when retinoids were used in combination with other chemotherapeutic agents, such as interferon-α and paclitaxel (DiPaola et al 1997, Culine et al 1999, Thaller et al 2000.…”

Section: Introductionmentioning

confidence: 99%

Vitamin A and apoptosis in prostate cancer.

2002

Endocrine-Related Cancer

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Apoptosis represents an effective way to eliminate cancer cells. Unfortunately, advanced prostate tumors eventually progress to androgen-independent tumors, which are resistant to current therapeutic approaches that act by triggering apoptosis. Vitamin A and its natural and synthetic analogs (retinoids) induce apoptosis in prostate cancer cells in vitro and in animal models, mainly through induction of retinoic acid receptor-β (RARβ). Expression levels of RARβ, however, are significantly reduced in hormone-independent prostate cancer cells. Recently, a new class of synthetic retinoids related to 6-[3-(1-adamantyl)-4-hydroxyphenyl]-2-naphthalene carboxylic acid (AHPN) (also called CD437) that effectively induces apoptosis of both hormone-dependent and -independent prostate cancer cells in a retinoid receptor-independent manner was identified and has drawn a lot of attention in the field. The apoptotic effect of AHPN requires expression of orphan receptor TR3 (also called nur77 or NGFI-B). Paradoxically, TR3 expression is also induced by androgen and other mitogenic agents in prostate cancer cells to confer their proliferation. The recent finding that TR3 migrates from the nucleus to mitochondria to trigger apoptosis in response to AHPN suggests that the opposing biological activities of TR3 are regulated by its subcellular localization. Thus, agents that induce translocalization of TR3 from the nucleus to mitochondria will have improved efficacy against prostate cancer. TR3, therefore, represents an unexplored molecule that may be an ideal target for developing new agents for prostate cancer therapy.

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Retinoid and androgen regulation of cell growth, epidermal growth factor and retinoic acid receptors in normal and carcinoma rat prostate cells

Cited by 25 publications

References 23 publications

Epigallocatechin‐3‐gallate and bicalutamide cause growth arrest and apoptosis in NRP‐152 and NRP‐154 prostate epithelial cells

Epigallocatechin‐3‐gallate and bicalutamide cause growth arrest and apoptosis in NRP‐152 and NRP‐154 prostate epithelial cells

Retinoic acid induces prostatic bud formation

Vitamin A and apoptosis in prostate cancer.

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