2015
DOI: 10.1158/1078-0432.ccr-15-0157
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SRRM4 Expression and the Loss of REST Activity May Promote the Emergence of the Neuroendocrine Phenotype in Castration-Resistant Prostate Cancer

Abstract: Purpose The neuroendocrine (NE) phenotype is associated with the development of metastatic castration-resistant prostate cancer (CRPC). Our objective was to characterize the molecular features of the NE phenotype in CRPC. Experimental Design Expression of chromogranin A (CHGA), synaptophysin (SYP), androgen receptor (AR), and prostate-specific antigen (PSA) was analyzed by immunohistochemistry (IHC) in 155 CRPC metastases from 50 patients and in 24 LuCaP prostate cancer patient-derived xenografts (PDX). Seve… Show more

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Cited by 151 publications
(175 citation statements)
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“…The cell numbers were measured using Alamar Blue ® cell viability assay and the fold difference is plotted on the Y-axis. D. NE1.3 cells expressing Scramble or shGKR3 were either untreated (UT) or treated with beta-adrenergic receptor antagonist, propranolol (PROP, dissolved in H 2 O, 10 μM, 4 hours), followed by western blotting analysis for expression of NE markers synaptophysin (SYP) and tubulin-beta III (TUBB3) [81, 82]. E. RT-PCR comparing the expression of NE markers in LNCaP cells upon overexpression of GFP, GRK3 (wild-type) or GRK3-KD (kinase dead) cDNA.…”
Section: Resultsmentioning
confidence: 99%
“…The cell numbers were measured using Alamar Blue ® cell viability assay and the fold difference is plotted on the Y-axis. D. NE1.3 cells expressing Scramble or shGKR3 were either untreated (UT) or treated with beta-adrenergic receptor antagonist, propranolol (PROP, dissolved in H 2 O, 10 μM, 4 hours), followed by western blotting analysis for expression of NE markers synaptophysin (SYP) and tubulin-beta III (TUBB3) [81, 82]. E. RT-PCR comparing the expression of NE markers in LNCaP cells upon overexpression of GFP, GRK3 (wild-type) or GRK3-KD (kinase dead) cDNA.…”
Section: Resultsmentioning
confidence: 99%
“…In addition to the N-myc/PTEN [27], N-myc/AKT [26], and the TP53/RB1 model [36-39] systems that drive NEPC, enzalutamide resistant models [40, 41], patient-derived xenograft (PDX) models [42, 43] and patient-derived organoids [44, 45] may be used to study drug resistance and the development of NEPC [42, 43]. Preclinical observations using these model systems combined with evaluation of additional patient samples have elucidated additional NEPC associated biologic pathways.…”
Section: Neuroendocrine Prostate Cancermentioning
confidence: 99%
“…The neuroendocrine phenotype is significantly associated with lower AR expression [11]. However, some reports indicate that AR expression might be retained in a relevant fraction of NEPCs [12,13]. NEPC is characterized by positive immunohistochemical (IHC) staining for CHGA, SYP, and neuronspecific enolase.…”
Section: Neuroendocrine Prostate Cancer: Clinical and Molecular Featuresmentioning
confidence: 99%
“…PcGs) are hyper-activated during NEPC progression, others might be suppressed. The loss of the REST gene in CRPC promotes NEPC development [12]. REST is part of the KDM1A-coREST-REST (Lysine-specific histone demethylase 1A-REST Corepressor 1-RE1-silencing transcription factor) histone modifying complex which is bound by HOTAIR, a long intergenic ncRNA that coordinates histone H3 lysine 27 methylation and lysine 4 demethylation [54].…”
Section: The Epigenetic/non-coding Interactome and Its Implication Inmentioning
confidence: 99%