Receptors, Androgen

Publication Title: 
Neuromolecular Medicine

DNA methylation, which is the transference of a methyl group to the 5'-carbon position of the cytosine in a CpG dinucleotide, is one of the major mechanisms of epigenetic modifications. A number of studies have demonstrated altered DNA methylation of peripheral blood cells in schizophrenia (SCZ) in previous studies.

Author(s): 
Kinoshita, Makoto
Numata, Shusuke
Tajima, Atsushi
Ohi, Kazutaka
Hashimoto, Ryota
Shimodera, Shinji
Imoto, Issei
Takeda, Masatoshi
Ohmori, Tetsuro
Publication Title: 
Cancer Research

Guggulsterone, a constituent of Indian Ayurvedic medicinal plant Commiphora mukul, causes apoptosis in cancer cells but the sequence of events leading to cell death is poorly understood. We now show that guggulsterone-induced cell death in human prostate cancer cells is caused by reactive oxygen intermediate (ROI)-dependent activation of c-Jun NH(2)-terminal kinase (JNK).

Author(s): 
Singh, Shivendra V.
Choi, Sunga
Zeng, Yan
Hahm, Eun-Ryeong
Xiao, Dong
Publication Title: 
Cancer Research

Guggulsterone, a constituent of Indian Ayurvedic medicinal plant Commiphora mukul, causes apoptosis in cancer cells but the sequence of events leading to cell death is poorly understood. We now show that guggulsterone-induced cell death in human prostate cancer cells is caused by reactive oxygen intermediate (ROI)-dependent activation of c-Jun NH(2)-terminal kinase (JNK).

Author(s): 
Singh, Shivendra V.
Choi, Sunga
Zeng, Yan
Hahm, Eun-Ryeong
Xiao, Dong
Publication Title: 
Cancer Research

Most prostate cancer patients develop androgen-independent recurrent prostate tumors a few years after androgen ablation therapy. No therapy, however, has been shown to substantially extend survival in these patients. Previously, we reported that androgen suppresses the growth of androgen-independent LNCaP prostate tumor cells both in vitro and in vivo. In cell culture, androgen receptor (AR)-rich androgen-independent LNCaP 104-R1 cells adapt to growth suppression by androgen and then their growth is androgen stimulated.

Author(s): 
Chuu, Chih-Pin
Hiipakka, Richard A.
Fukuchi, Junichi
Kokontis, John M.
Liao, Shutsung
Publication Title: 
Cancer Research

1,25-Dihydroxyvitamin D3 [1,25(OH)2D3], the active metabolite of vitamin D3, inhibits the proliferation of prostate cancer cells. However, the molecular mechanisms by which 1,25(OH)2D3 inhibits the proliferation of these cells remain to be fully elucidated. In this study, we used microarray technology to identify target genes of 1,25(OH)2D3 in androgen-responsive prostate cancer LNCaP cells. 1,25(OH)2D3 up-regulated CCAAT/enhancer-binding protein delta (C/EBPdelta) by approximately 5-fold in these cells.

Author(s): 
Ikezoe, Takayuki
Gery, Sigal
Yin, Dong
O'Kelly, James
Binderup, Lise
Lemp, Nathan
Taguchi, Hirokuni
Koeffler, H. Phillip
Publication Title: 
Cancer Research

Androgen-dependent human LNCaP 104-S tumor xenografts progressed to androgen-independent relapsed tumors (104-Rrel) in athymic mice after castration. The growth of 104-Rrel tumors was suppressed by testosterone. However, 104-Rrel tumors adapted to androgen and regrew as androgen-stimulated 104-Radp tumors. Androgen receptor expression in tumors and serum prostate-specific antigen increased during progression from 104-S to 104-Rrel but decreased during transition from 104-Rrel to 104-Radp. Expression of genes related to liver X receptor (LXR) signaling changed during progression.

Author(s): 
Chuu, Chih-Pin
Hiipakka, Richard A.
Kokontis, John M.
Fukuchi, Junichi
Chen, Rou-Yu
Liao, Shutsung
Publication Title: 
Biochemical and Biophysical Research Communications

T0901317 is a potent non-steroidal synthetic liver X receptor (LXR) agonist. T0901317 blocked androgenic stimulation of the proliferation of androgen-dependent LNCaP 104-S cells and androgenic suppression of the proliferation of androgen-independent LNCaP 104-R2 cells, inhibited the transcriptional activation of an androgen-dependent reporter gene by androgen, and suppressed gene and protein expression of prostate specific antigen (PSA), a target gene of androgen receptor (AR) without affecting gene and protein expression of AR.

Author(s): 
Chuu, Chih-Pin
Chen, Rou-Yu
Hiipakka, Richard A.
Kokontis, John M.
Warner, Karen V.
Xiang, Jialing
Liao, Shutsung
Publication Title: 
Cancer Letters

The green tea polyphenol, (-)-epigallocatechin-3-gallate (EGCG), inhibits the development and progression of prostate cancer in TRAMP mice and in men. We examined the effects of EGCG on LNCaP human prostate cancer sublines 104-S, 104-R1 and R1Ad representing different progression stages of prostate cancer. EGCG suppressed cell proliferation, prostate specific antigen (PSA) expression, and AR transcriptional activity in the different LNCaP sublines. Intraperitoneal administration of EGCG also suppressed the growth of relapsing R1Ad tumors and decreased tumor-derived serum PSA.

Author(s): 
Chuu, Chih-Pin
Chen, Rou-Yu
Kokontis, John M.
Hiipakka, Richard A.
Liao, Shutsung
Publication Title: 
Endocrinology

beta-Catenin/T-cell factor signaling (beta-CTS) plays multiple critical roles in carcinogenesis and is blocked by androgens in androgen receptor (AR)-responsive prostate cancer (PrCa) cells, primarily via AR sequestration of beta-catenin from T-cell factor. Dehydroepiandrosterone (DHEA), often used as an over-the-counter nutritional supplement, is metabolized to androgens and estrogens in humans. The efficacy and safety of unregulated use of DHEA are unclear.

Author(s): 
Liu, Xunxian
Arnold, Julia T.
Blackman, Marc R.
Publication Title: 
The Prostate

BACKGROUND: Prostate cancer (PrCa) risk is positively associated with levels of insulin-like growth factor I (IGF-I) and prostate specific antigen (PSA), both androgen receptor (AR) signaling target genes in PrCa cells. Although activated AR is required for androgen-induction of expression of both genes, effects of the IGF-I signaling pathways on the androgen-induction of PSA have not been studied. METHODS: Human prostate stromal and epithelial cancer cells were treated alone or in coculture with steroid hormone and/or inhibitors.

Author(s): 
Liu, Xunxian
Choi, Renee Y.
Jawad, Shayma M.
Arnold, Julia T.

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