scholarly journals Reshaping of the androgen-driven chromatin landscape in normal prostate cells by early cancer drivers and effect on therapeutic sensitivity

Cell Reports ◽  
2021 ◽  
Vol 36 (10) ◽  
pp. 109625 ◽  
Author(s):  
Ivana Grbesa ◽  
Michael A. Augello ◽  
Deli Liu ◽  
Dylan R. McNally ◽  
Christopher D. Gaffney ◽  
...  
Keyword(s):  
Early Cancer ◽  
Normal Prostate ◽  
Prostate Cells ◽  
Cancer Drivers

AS1 expression in prostate cancer and its effects on proliferation and invasion of prostate cancer cells

2021 ◽  
pp. 1-9
Author(s):  
Yuxin Li ◽  
Xiaohong Zhuang ◽  
Li Zhuang ◽  
Hongjian Liu
Keyword(s):  
Prostate Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Related Protein ◽  
Prostate Cancer Cells ◽  
Blank Group ◽  
Normal Prostate ◽  
Cell Cycles ◽  
Prostate Cells ◽  
Proliferation And Invasion

This paper aimed at investigating AS1 expression in prostate cancer (PCa) and its effects on the proliferation and invasion of prostate cancer cells (PCCs). The prostate tissues and the matched adjacent normal prostate tissues excised and preserved during radical prostatectomy in our hospital were collected. The LncRNA NCK1-AS1 expression was detected. PCa patients were followed up for three years to analyze their prognosis. The correlation of LncRNA NCK1-AS1 expression with clinicopathological features was analyzed. Human normal prostate cells and human PCCs were selected, in which LncRNA NCK1-AS1 expression was tested to screen and then transfect the cells. Cell proliferation, invasion and migration were detected. Cell cycles and apoptosis were analyzed. Compared with the adjacent normal tissues, LncRNA NCK1-AS1 was highly expressed in the prostate cancer tissues. Its expression was remarkably different in those with different stages of TNM and with lymphatic metastasis or not. The prognosis of patients with high LncRNA NCK1-AS1 expression was remarkably poorer than that of those with low expression. Compared with the human normal prostate cells, LncRNA NCK1-AS1 expression in the human PCCs remarkably rose, with the greatest difference in 22Rv1 cells. Compared with the Blank group, cell proliferation and the number of plate cloned cells remarkably reduced in the sh-NCK1-AS1 group. Additionally, in this group, the number of invasive and migratory cells remarkably reduced; the expression of invasion-related protein E-cadherin remarkably rose but that of MMP-2 remarkably reduced; cell cycles were arrested and the expression of cycle-related proteins (CDK4, CDK6, cyclin D1) remarkably reduced; the apoptotic rate and the expression of apoptosis-related protein Bax remarkably rose. LncRNA NCK1-AS1 is highly expressed in PCa, so its down-regulation can inhibit PCCs from proliferating and reduce the number of invasive cells.

scholarly journals Prostate Stem Cells in the Development of Benign Prostate Hyperplasia and Prostate Cancer: Emerging Role and Concepts

2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Akhilesh Prajapati ◽  
Sharad Gupta ◽  
Bhavesh Mistry ◽  
Sarita Gupta
Keyword(s):  
Prostate Cancer ◽  
Stem Cells ◽  
Benign Prostate Hyperplasia ◽  
Normal Prostate ◽  
Prostate Hyperplasia ◽  
Regulatory Factors ◽  
Prostate Cells ◽  
Hormonal Imbalance ◽  
Benign Prostate ◽  
Insight Into

Benign Prostate hyperplasia (BPH) and prostate cancer (PCa) are the most common prostatic disorders affecting elderly men. Multiple factors including hormonal imbalance, disruption of cell proliferation, apoptosis, chronic inflammation, and aging are thought to be responsible for the pathophysiology of these diseases. Both BPH and PCa are considered to be arisen from aberrant proliferation of prostate stem cells. Recent studies on BPH and PCa have provided significant evidence for the origin of these diseases from stem cells that share characteristics with normal prostate stem cells. Aberrant changes in prostate stem cell regulatory factors may contribute to the development of BPH or PCa. Understanding these regulatory factors may provide insight into the mechanisms that convert quiescent adult prostate cells into proliferating compartments and lead to BPH or carcinoma. Ultimately, the knowledge of the unique prostate stem or stem-like cells in the pathogenesis and development of hyperplasia will facilitate the development of new therapeutic targets for BPH and PCa. In this review, we address recent progress towards understanding the putative role and complexities of stem cells in the development of BPH and PCa.

scholarly journals Cytochrome P450 3A5 is highly expressed in normal prostate cells but absent in prostate cancer

2007 ◽  
Vol 14 (3) ◽  
pp. 645-654 ◽  
Author(s):  
S Leskelä ◽  
E Honrado ◽  
C Montero-Conde ◽  
I Landa ◽  
A Cascón ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cytochrome P450 ◽  
Prostate Cancer Risk ◽  
Cytochrome P450 3A ◽  
Active Metabolites ◽  
Normal Prostate ◽  
Prostate Cells ◽  
Mrna Content ◽  
Luminal Cells ◽  
And Function

Testosterone is essential for the growth and function of the luminal prostate cells, but it is also critical for the development of prostate cancer, which in the majority of the cases derives from luminal cells. Cytochrome P450 3A (CYP3A) enzymes hydroxylate testosterone and dehydroepiandrosterone to less active metabolites, which might be the basis for the association between CYP3A polymorphisms and prostate cancer. However, it is unknown whether the CYP3A enzymes are expressed at relevant levels in the prostate and which polymorphisms could affect this tissue-specific CYP3A activity. Thus, we measured CYP3A4, CYP3A5, CYP3A7, and CYP3A43 mRNA in 14 benign prostatic hyperplasias and ten matched non-tumoral/tumoral prostate samples. We found that CYP3A5 mRNA in non-tumoral prostate tissue was 10% of the average amount of liver samples, whereas the expression of the other CYP3A genes was much lower. Similarly to liver, CYP3A5*3 polymorphism decreased CYP3A5 mRNA content 13-fold. CYP3A5 protein was detected in non-tumoral prostate microsomes by western blot, and immunohistochemistry (IHC) localized CYP3A5 exclusively in the basolateral prostate cells. In contrast to the normal tissue, IHC and RT-PCR showed that tumoral tissue lacked CYP3A5 expression. In conclusion, prostate basolateral cells express high levels of CYP3A5 which dramatically decrease in tumoral tissue. This finding supports an endogenous function of CYP3A5 related to the metabolism of intra-prostatic androgens and cell growth, and that polymorphisms affecting CYP3A5 activity may result in altered prostate cancer risk and aggressiveness.

The 2013 Young Investigator Grant – Effects of non-target dose on normal prostate cells

2014 ◽  
Vol 30 (6) ◽  
pp. 720
Author(s):  
Laura Shields ◽  
Brendan Mc Clean
Keyword(s):  
Target Dose ◽  
Young Investigator ◽  
Normal Prostate ◽  
Prostate Cells

scholarly journals Reducing Selenoprotein F Promotes the Transformation of Immortalized Prostate Epithelial Cells

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 1809-1809
Author(s):  
Lenny Hong ◽  
Mostafa Elhodaky ◽  
Shrinidhi Kadkol ◽  
Alan Diamond
Keyword(s):  
Prostate Cancer ◽  
Epithelial Cells ◽  
Cancer Progression ◽  
Tca Cycle ◽  
Soft Agar ◽  
Metabolic Shift ◽  
Normal Prostate ◽  
Funding Sources ◽  
Prostate Cells ◽  
Prostate Epithelial Cells

Abstract Objectives Selenoprotein F (SELENOF) levels are responsive to available dietary selenium and found in high levels in benign prostate cells. It is implicated in prostate cancer (PCa) mortality due to associations between polymorphisms in the corresponding gene and death from the disease. SELENOF levels are dramatically lower in prostate cancer compared to adjacent benign tissue. The objective of this study was to determine whether reducing SELENOF levels in human, non-transformed RWPE-1 prostate epithelial cells alters their phenotype to implicate SELENOF loss in PCa progression. Methods SELENOF levels were reduced in RWPE-1 cells that express high levels of SELENOF using a SELENOF shRNA construct. Proliferation was determined by quantifying DNA using fluorometric dsDNA quantitation. Growth in soft agar and cell mobility of cells in culture (wound healing assay) were imaged using an Evos FL microscope and quantified using Image J software. The oxygen consumption rate (OCR) was measured using a Seahorse XFe24 Analyzer. Results SELENOF levels were reduced in RWPE-1 and these cells exhibited decreased contact inhibition in culture (n = 3, P < 0.001) when compared to controls. Normal prostate epithelial cells are atypical in that they rely on glycolysis for energy production, have a truncated TCA cycle, and a metabolic shift from glycolysis to oxidative phosphorylation (OXPHOS) occurs in PCa. Reducing SELENOF in RWPE-1 cells resulted in higher OCR compared to controls, indicating that SELENOF can impact the sources and pathways used in cellular energy metabolism. Conclusions Reduced SELENOF levels in RWPE-1 prostate cells resulted in properties consistent with a transformed phenotype and an increase in OCR, and indicating that the reduction in SELENOF may contribute a metabolic shift towards a PCa cancer-like metabolism. Together, these results indicate that SELENOF loss likely contributes to cancer progression. Funding Sources This work was supported by a grant from the Department of Defense to AMD and a Pre-Doctoral Education for Clinical and Translational Scientists Fellowship to LKH.

A simple approach to room-temperature synthesis of cubic Al-doped HfO2 nanoparticles and their toxicity evaluation in normal prostate cells

2020 ◽  
Vol 274 ◽  
pp. 128048
Author(s):  
D. Salado-Leza ◽  
E. Mendoza-Mendoza ◽  
J.A. Castillo-Ramírez ◽  
C. Escudero-Lourdes ◽  
L.A. García-Cerda
Keyword(s):  
Room Temperature ◽  
Simple Approach ◽  
Toxicity Evaluation ◽  
Temperature Synthesis ◽  
Normal Prostate ◽  
Room Temperature Synthesis ◽  
Prostate Cells

Potential role of CFTR in bisphenol A-induced malignant transformation of prostate cells via mitochondrial apoptosis

2020 ◽  
Vol 36 (8) ◽  
pp. 531-539
Author(s):  
Jia Liu ◽  
Chaoyan Ou ◽  
Xiaonian Zhu ◽  
Chao Tan ◽  
Xuebao Xiang ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Bisphenol A ◽  
Malignant Transformation ◽  
Potential Role ◽  
Annexin V ◽  
Mitochondrial Apoptosis ◽  
Normal Prostate ◽  
Prostate Cells ◽  
Significant Difference

Bisphenol A (BPA) is an environmental endocrine disruptor and a risk factor for prostate cancer. The cystic fibrosis transmembrane conductance regulator (CFTR) is proposed to be a prostate cancer suppressor in some recent researches. However, the potential role and mechanism of CFTR in BPA-induced prostate cancer cells has not been well identified. In this study, BPA decreased the viability of human normal prostate RWPE-1 cells detected with a CCK-8 kit. The capacity of the cell line on soft agar colony formation, wound healing, and transwell invasion indicated malignant transformation induced by BPA. Western blot analysis demonstrated that the levels of CFTR and Bcl-2 decreased, whereas Bax level increased, and ELISA detection showed a decreased ATP level in BPA-exposed cells. Cell apoptosis was analyzed with Annexin V-FITC Detection Kit by flow cytometry. However, no significant difference was observed in cell viability and apoptosis rates compared to normal RWPE-1 cells. Our research revealed a potential role of CFTR in BPA-induced malignant transformation via mitochondrial apoptosis of normal prostate cells.

scholarly journals Increased distributional variance of mitochondrial DNA content associated with prostate cancer cells as compared with normal prostate cells

The Prostate ◽  
2008 ◽  
Vol 68 (4) ◽  
pp. 408-417 ◽  
Author(s):  
Takatsugu Mizumachi ◽  
Levan Muskhelishvili ◽  
Akihiro Naito ◽  
Jun Furusawa ◽  
Chun-Yang Fan ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Mitochondrial Dna ◽  
Cancer Cells ◽  
Dna Content ◽  
Prostate Cancer Cells ◽  
Normal Prostate ◽  
Prostate Cells ◽  
Mitochondrial Dna Content

scholarly journals Annexin-A7 protects normal prostate cells and induces distinct patterns of RB-associated cytotoxicity in androgen-sensitive and -resistant prostate cancer cells

2009 ◽  
Vol 125 (11) ◽  
pp. 2528-2539 ◽  
Author(s):  
Yelizaveta Torosyan ◽  
Olga Simakova ◽  
Shanmugam Naga ◽  
Katerina Mezhevaya ◽  
Ximena Leighton ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Prostate Cancer Cells ◽  
Normal Prostate ◽  
Prostate Cells ◽  
Annexin A7
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