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10.1002/pros.22828 http://scihub22266oqcxt.onion/10.1002/pros.22828 C4856018!4856018!24913829     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=24913829&cmd=llinks): Failed to open stream: HTTP request failed! 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Androgen Receptor (AR) Suppresses Normal Human Prostate Epithelial Cell Proliferation via AR/?-catenin/TCF-4 Complex Inhibition of c-MYC Transcription |pdf=|usr=}}{{24913829}} gab.com Text Androgen Receptor (AR) Suppresses Normal Human Prostate Epithelial Cell Proliferation via AR/ -catenin/TCF-4 Complex Inhibition of c-MYC Transcription JO: Prostate http://www.kidney.de/pget.php?&tw=1&pmid=24913829 #FOAvip INTRODUCTION: Physiologic testosterone continuously stimulates prostate stromal cell secretion of paracrine growth factors (PGFs), which if unopposed would induce hyperplastic overgrowth of normal prostate epithelial cells (PrECs). METHODS: Lentiviral shRNA stable knock down of c-MYC, ?-catenin, or TCF-4 completely inhibits normal (i.e., non-transformed) human PrECs growth. c-MYC enhancer driven reporter expression and growth is inhibited by two chemically distinct molecules, which prevent ?-catenin signaling either by blocking TCF-4 binding (i.e., toxoflavin) or by stimulating degradation (i.e., AVX939). Recombinant DKK1 protein at a dose, which inhibits activation of canonical Wnt signaling does not inhibit PrEC growth. Nuclear ?-catenin translocation and PrEC growth is prevented by both lack of PGFs or Akt inhibitor-I. Growth inhibition induced by lack of PGFs, toxoflavin, or Akt inhibitor-I is overcome by constitutive c-MYC transcription. RESULTS: In the presence of continuous PGF signaling, PrEC hyperplasia is prevented by androgen binding to AR suppressing c-MYC transcription, resulting in G0 arrest/terminal differentiation independent of Rb, p21, p27, FoxP3, or down regulation of growth factors receptors and instead involves androgen-induced formation of AR/?-catenin/TCF-4 complexes, which suppress c-MYC transcription. Such suppression does not occur when AR is mutated in its zinc-finger binding domain. DISCUSSION: Proliferation of non-transformed human PrECs is dependent upon c-MYC transcription via formation/binding of ?-catenin/TCF-4 complexes at both 5? and 3? c-MYC enhancers stimulated by Wnt-independent, PGF induced Akt signaling. In the presence of continuous PGF signaling, PrEC hyperplasia is prevented by androgen-induced formation of AR/?-catenin/TCF-4 complexes, which retains binding to 3? c-MYC enhancer, but now suppresses c-MYC transcription. Twit Text FOAVip Androgen Receptor (AR) Suppresses Normal Human Prostate Epithelial Cell Proliferation via AR/ -catenin/TCF-4 Complex Inhibition of c-MYC Transcription ????Prostate http://www.kidney.de/pget.php?&tw=1&pmid=24913829 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24913829 #FOAvip English Wikipedia <ref>{{Cite pmid|24913829}}</ref> Androgen Receptor (AR) Suppresses Normal Human Prostate Epithelial Cell Proliferation via AR/?-catenin/TCF-4 Complex Inhibition of c-MYC Transcription #MMPMID24913829 Antony L; van der Schoor F; Dalrymple SL; Isaacs JT Prostate 2014[Aug]; 74 (11): 1118-31 PMID24913829show ga INTRODUCTION: Physiologic testosterone continuously stimulates prostate stromal cell secretion of paracrine growth factors (PGFs), which if unopposed would induce hyperplastic overgrowth of normal prostate epithelial cells (PrECs). METHODS: Lentiviral shRNA stable knock down of c-MYC, ?-catenin, or TCF-4 completely inhibits normal (i.e., non-transformed) human PrECs growth. c-MYC enhancer driven reporter expression and growth is inhibited by two chemically distinct molecules, which prevent ?-catenin signaling either by blocking TCF-4 binding (i.e., toxoflavin) or by stimulating degradation (i.e., AVX939). Recombinant DKK1 protein at a dose, which inhibits activation of canonical Wnt signaling does not inhibit PrEC growth. Nuclear ?-catenin translocation and PrEC growth is prevented by both lack of PGFs or Akt inhibitor-I. Growth inhibition induced by lack of PGFs, toxoflavin, or Akt inhibitor-I is overcome by constitutive c-MYC transcription. RESULTS: In the presence of continuous PGF signaling, PrEC hyperplasia is prevented by androgen binding to AR suppressing c-MYC transcription, resulting in G0 arrest/terminal differentiation independent of Rb, p21, p27, FoxP3, or down regulation of growth factors receptors and instead involves androgen-induced formation of AR/?-catenin/TCF-4 complexes, which suppress c-MYC transcription. Such suppression does not occur when AR is mutated in its zinc-finger binding domain. DISCUSSION: Proliferation of non-transformed human PrECs is dependent upon c-MYC transcription via formation/binding of ?-catenin/TCF-4 complexes at both 5? and 3? c-MYC enhancers stimulated by Wnt-independent, PGF induced Akt signaling. In the presence of continuous PGF signaling, PrEC hyperplasia is prevented by androgen-induced formation of AR/?-catenin/TCF-4 complexes, which retains binding to 3? c-MYC enhancer, but now suppresses c-MYC transcription. äAndrogen Receptor (AR) Suppresses Normal Human Prostate Epithelial Cel(epmc).pdf DeepDyve Pubget Overpricing