The Role of I Kappa B Kinases in Prostate Carcinogenesis and the Effect oh Their Inhibition on Survival of Prostate Tumors

2006 ◽  
Author(s):  
Michael Karin
Keyword(s):  
Prostate Tumors ◽  
Prostate Carcinogenesis

scholarly journals The role of SPARC in the TRAMP model of prostate carcinogenesis and progression

Oncogene ◽  
2009 ◽  
Vol 28 (39) ◽  
pp. 3487-3498 ◽  
Author(s):  
N Said ◽  
H F Frierson ◽  
D Chernauskas ◽  
M Conaway ◽  
K Motamed ◽  
...  
Keyword(s):  
Prostate Carcinogenesis

scholarly journals Does Physical Activity Regulate Prostate Carcinogenesis and Prostate Cancer Outcomes? A Narrative Review

2020 ◽  
Vol 17 (4) ◽  
pp. 1441 ◽  
Author(s):  
Marco Capece ◽  
Massimiliano Creta ◽  
Armando Calogero ◽  
Roberto La Rocca ◽  
Luigi Napolitano ◽  
...  
Keyword(s):  
Physical Activity ◽  
Prostate Cancer ◽  
Functional Outcomes ◽  
Narrative Review ◽  
Common Disease ◽  
Prostate Carcinogenesis ◽  
Patients At Risk ◽  
The Impact ◽  
Circulating Levels

Background: Prostate cancer (PCa) represents a common disease in men aged >65 years. The role of physical activity (PA) in patients at risk or diagnosed with PCa represents an evolving issue. We aimed to summarize available evidences about the impact of PA on the pathophysiology and clinical outcomes of PCa. Methods: We performed a narrative review. Evidences about the role of PA in elderly patients in terms of PCa biology, epidemiology, oncological and functional outcomes, as well as in terms of impact on the outcomes of androgen deprivation therapy (ADT) were summarized. Results: Potential pathophysiological pathways hypothesized to explain the benefits of PA in terms of prostate carcinogenesis include circulating levels of Insulin-like growth factor-1 (IGF-1), oxidative stress, systemic inflammation, sex hormones, and myokines. Clinically, emerging evidences support the hypothesis that PA is associated with decreased PCa risk, improved PCa-related survival, improved functional outcomes, and reduced ADT-related adverse events.

Abstract 535: The role of high mobility group box 1 (HMGB1) in prostate carcinogenesis

2012 ◽  
Author(s):  
Purvi Patel ◽  
Michelle Zheng ◽  
Maarten C. Bosland ◽  
André Kajdacsy-Balla ◽  
Gnanasekar Munirathinam
Keyword(s):  
High Mobility ◽  
High Mobility Group ◽  
Prostate Carcinogenesis

Dynamic contrast-enhanced (DCE) MR imaging: the role of qualitative and quantitative parameters for evaluating prostate tumors stratified by Gleason score and PI-RADS v2

2019 ◽  
Vol 45 (7) ◽  
pp. 2225-2234 ◽  
Author(s):  
Sohrab Afshari Mirak ◽  
Amirhossein Mohammadian Bajgiran ◽  
Kyunghyun Sung ◽  
Nazanin H. Asvadi ◽  
Daniela Markovic ◽  
...  
Keyword(s):  
Mr Imaging ◽  
Gleason Score ◽  
Prostate Tumors ◽  
Qualitative And Quantitative ◽  
Dynamic Contrast Enhanced ◽  
Quantitative Parameters ◽  
Contrast Enhanced

scholarly journals Role of Estrogen in Androgen-Induced Prostate Carcinogenesis in NBL Rats

2019 ◽  
Vol 10 (2-3) ◽  
pp. 77-88 ◽  
Author(s):  
Nur Ozten ◽  
Katherine Vega ◽  
Joachim Liehr ◽  
Xi Huang ◽  
Lori Horton ◽  
...  
Keyword(s):  
Prostate Carcinogenesis

scholarly journals ERβ and NFκB—Modulators of Zearalenone-Induced Oxidative Stress in Human Prostate Cancer Cells

Toxins ◽  
2020 ◽  
Vol 12 (3) ◽  
pp. 199 ◽  
Author(s):  
Karolina Kowalska ◽  
Dominika Ewa Habrowska-Górczyńska ◽  
Kamila Domińska ◽  
Kinga Anna Urbanek ◽  
Agnieszka Wanda Piastowska-Ciesielska
Keyword(s):  
Oxidative Stress ◽  
Prostate Cancer ◽  
Cancer Cells ◽  
Prostate Cancer Cells ◽  
M Cell ◽  
Androgen Independence ◽  
Prostate Carcinogenesis ◽  
Cycle Arrest ◽  
Light Chain Enhancer

Nuclear factor kappa-light-chain-enhancer of activated B cells (NFκB) is commonly expressed in prostate cancer (PCa) cells and is associated with increased proliferation, metastases and androgen independence. Zearalenone (ZEA) is one of the most common mycotoxins contaminating food, which might mimic estrogens and bind to estrogen receptors (ERs). The ratio of androgens to estrogens in men decreases physiologically with age, and is believed to participate in prostate carcinogenesis. In this study, we evaluated the role of NFκB and ERβ in the induction of oxidative stress in human PCa cells by ZEA. As observed, ZEA at a dose of 30 µM induces oxidative stress in PCa cells associated with DNA damage and G2/M cell cycle arrest. We also observed that the inhibition of ERβ and NFΚB via specific inhibitors (PHTPP and BAY 117082) significantly increased ZEA-induced oxidative stress, although the mechanism seems to be different for androgen-dependent and androgen-independent cells. Based on our findings, it is possible that the activation of ERβ and NFΚB in PCa might protect cancer cells from ZEA-induced oxidative stress. We therefore shed new light on the mechanism of ZEA toxicity in human cells.

scholarly journals Androgen deprivation induces human prostate epithelial neuroendocrine differentiation of androgen-sensitive LNCaP cells

2006 ◽  
Vol 13 (1) ◽  
pp. 151-167 ◽  
Author(s):  
Ta-Chun Yuan ◽  
Suresh Veeramani ◽  
Fen-Fen Lin ◽  
Dmitry Kondrikou ◽  
Stanislav Zelivianski ◽  
...  
Keyword(s):  
Specific Antigen ◽  
Neuron Specific Enolase ◽  
Neuronal Morphology ◽  
Receptor Protein ◽  
Lncap Cells ◽  
Normal Prostate ◽  
Androgen Ablation ◽  
Prostate Carcinogenesis ◽  
Hormone Refractory

Neuroendocrine (NE) cells are the minor cell populations in normal prostate epithelial compartments. During prostate carcinogenesis, the number of NE cells in malignant lesions increases, correlating with its tumorigenicity and hormone-refractory growth. It is thus proposed that cancerous NE cells promote prostate cancer (PCa) cell progression and its androgen-independent proliferation, although the origin of the cancerous NE cells is not clear. To investigate the role of cancerous NE cells in prostate carcinogenesis, we characterized three NE subclone cell lines–NE-1.3, NE-1.8 and NE-1.9, which were transdifferentiated from androgen-sensitive human PCa LNCaP cells by culturing in an androgen-depleted environment, resembling clinical androgen-ablation therapy. These subclone cells acquire many features of NE cells seen in clinical prostate carcinomas, for example exhibiting a neuronal morphology and expressing multiple NE markers, including neuron-specific enolase, chromogranin B, neurotensin, parathyroid hormone-related peptide, and to a lesser degree for chromogranin A, while lacking androgen receptor (AR) or prostate specific antigen (PSA) expression. These cells represent terminally differentiated stable cells because after 3 months of re-culturing in a medium containing androgenic activity, they still retained the NE phenotype and expressed NE markers. Despite these NE cells having a slow growth rate, they readily developed xenograft tumors. Furthermore, media conditioned by these NE cells exhibited a stimulatory effect on proliferation and PSA secretion by LNCaP cells in androgen-deprived conditions. Additionally, we found that receptor protein tyrosine phosphatase α plays a role in upregulating multiple NE markers and acquiring the NE phenotype. These NE cells thus represent cancerous NE cells and could serve as a useful cell model system for investigating the role of cancerous NE cells in hormone-refractory proliferation of PCa cells.

scholarly journals Androgen Receptor Signalling in Prostate Cancer: The Functional Consequences of Acetylation

2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Derek N. Lavery ◽  
Charlotte L. Bevan
Keyword(s):  
Prostate Cancer ◽  
Androgen Receptor ◽  
Cancer Progression ◽  
Histone Deacetylases ◽  
Transcriptional Response ◽  
Fine Tuning ◽  
Receptor Signalling ◽  
Prostate Carcinogenesis ◽  
Functional Consequences

The androgen receptor (AR) is a ligand activated transcription factor and member of the steroid hormone receptor (SHR) subfamily of nuclear receptors. In the early stages of prostate carcinogenesis, tumour growth is dependent on androgens, and AR directly mediates these effects by modulating gene expression. During transcriptional regulation, the AR recruits numerous cofactors with acetylation-modifying enzymatic activity, the best studied include p300/CBP and the p160/SRC family of coactivators. It is known that recruitment of histone acetyltransferases (HATs) and histone deacetylases (HDACs) is key in fine-tuning responses to androgens and is thus likely to play a role in prostate cancer progression. Further, these proteins can also modify the AR itself. The functional consequences of AR acetylation, the role of modifying enzymes in relation to AR transcriptional response, and prostate cancer will be discussed.

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