Prostate cancer

Summary

Prostate cancer is the uncontrolled growth of cells in the prostate, a gland in the male reproductive system just below the bladder. Early prostate cancer usually causes no symptoms. As the tumor grows, it can damage nearby organs causing erectile dysfunction, blood in the urine or semen, and trouble urinating. Some tumors eventually spread to other areas of the body, particularly the bones and lymph nodes. There, tumors cause severe bone pain, leg weakness or paralysis, and eventually death. Most cases of prostate cancer are detected by prostate cancer screening programs. These typically rely on regular blood tests for levels of prostate-specific antigen (PSA), which is elevated in those with prostate cancer or other conditions affecting the prostate. Screening can also involve a digital rectal exam to feel for prominent prostate tumors. A definitive diagnosis requires a biopsy of the prostate. A sample of the suspected tumor is examined by a pathologist under a microscope. If cance

Official source

https://en.wikipedia.org/wiki/Prostate_cancer

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Gene expression profiling of the stromal reaction to invasive human breast and prostate cancer

Anne Planche

Primary tumor growth induces host tissue responses that are believed to support and promote tumor progression. Identification of the molecular characteristics of the tumor microenvironment and a deeper knowledge of its crosstalk with tumor cells may therefore be crucial for improving our understanding of the processes implicated in cancer progression, for discovering potential therapeutic targets, and for finding a stromal signature that may predict clinical outcome. To selectively address stromal gene expression changes during cancer progression, oligo-based Affymetrix microarray technology was used to analyze laser-microdissected stromal cells derived from invasive human breast and prostate carcinoma in comparison to their normal counterparts. Statistical analysis of the gene expression profile of breast and prostate stroma revealed genes differentially expressed in tumor stroma compared to normal stroma together with genes common to the stromal reaction in both tumor types. Several up and downregulated genes were validated by quantitative real-time RT-PCR and one common upregulated gene, periostin (POSTN), was validated by immunohistochemistry. The tumor-specific stromal genes as well as common stromal genes were observed to cluster breast and prostate cancer patients into two groups with statistically different clinical outcome. Univariate Cox analysis identified the genes whose expression level was most strongly associated with patient survival. Taken together, these observations provide evidence of the implication of the tumor microenvironment in tumor progression and its survival-predictive value.

2008

Reduced NCOR2 expression accelerates androgen deprivation therapy failure in prostate cancer

Gerard Llimos Aubach

This study addresses the roles of nuclear receptor corepressor 2 (NCOR2) in prostate cancer (PC) progression in response to androgen deprivation therapy (ADT). Reduced NCOR2 expression significantly associates with shorter disease-free survival in patients with PC receiving adjuvant ADT. Utilizing the CWR22 xenograft model, we demonstrate that stably reduced NCOR2 expression accelerates disease recurrence following ADT, associates with gene expression patterns that include neuroendocrine features, and induces DNA hypermethylation. Stably reduced NCOR2 expression in isogenic LNCaP (androgen-sensitive) and LNCaP-C4-2 (androgen-independent) cells revealed that NCOR2 reduction phenocopies the impact of androgen treatment and induces global DNA hypermethylation patterns. NCOR2 genomic binding is greatest in LNCaP-C4-2 cells and most clearly associates with forkhead box (FOX) transcription factor FOXA1 binding. NCOR2 binding significantly associates with transcriptional regulation most when in active enhancer regions. These studies reveal robust roles for NCOR2 in regulating the PC transcriptome and epigenome and underscore recent mutational studies linking NCOR2 loss of function to PC disease progression.

CELL PRESS2021

Expression levels of retinoic acid receptor gamma (NR1B3/RARG, encodes RAR gamma) are commonly reduced in prostate cancer (PCa). Therefore, we sought to establish the cellular and gene regulatory consequences of reduced RAR gamma expression, and determine RAR gamma regulatory mechanisms. RARG shRNA approaches in non-malignant (RWPE-1 and HPr1-AR) and malignant (LNCaP) prostate models revealed that reducing RAR gamma levels, rather than adding exogenous retinoid ligand, had the greatest impact on prostate cell viability and gene expression. ChIP-Seq defined the RAR gamma cistrome, which was significantly enriched at active enhancers associated with AR binding sites. Reflecting a significant genomic role for RAR gamma to regulate androgen signaling, RAR gamma knockdown in HPr1-AR cells significantly regulated the magnitude of the AR transcriptome. RAR gamma downregulation was explained by increased miR-96 in PCa cell and mouse models, and TCGA PCa cohorts. Biochemical approaches confirmed that miR-96 directly regulated RAR gamma expression and function. Capture of the miR-96 targetome by biotin-miR-96 identified that RAR gamma and a number of RAR gamma interacting co-factors including TACC1 were all targeted by miR-96, and expression of these genes were prominently altered, positively and negatively, in the TCGA-PRAD cohort. Differential gene expression analyses between tumors in the TCGA-PRAD cohort with lower quartile expression levels of RARG and TACC1 and upper quartile miR-96, compared to the reverse, identified a gene network including several RAR gamma target genes (e.g., SOX15) that significantly associated with worse disease-free survival (hazard ratio 2.23, 95% CI 1.58 to 2.88, p = 0.015). In summary, miR-96 targets a RAR gamma network to govern AR signaling, PCa progression and disease outcome.

Springer2019