scholarly journals A comprehensive review of the role of zinc in normal prostate function and metabolism; and its implications in prostate cancer

2016 ◽  
Vol 611 ◽  
pp. 100-112 ◽  
Author(s):  
Leslie C. Costello ◽  
Renty B. Franklin
Keyword(s):  
Prostate Cancer ◽  
Normal Prostate ◽  
Comprehensive Review

scholarly journals The Role of Cancer-Associated Fibroblasts in Prostate Cancer Tumorigenesis

Cancers ◽  
2020 ◽  
Vol 12 (7) ◽  
pp. 1887 ◽  
Author(s):  
Francesco Bonollo ◽  
George N. Thalmann ◽  
Marianna Kruithof-de Julio ◽  
Sofia Karkampouna
Keyword(s):  
Prostate Cancer ◽  
Molecular Mechanisms ◽  
Therapeutic Potential ◽  
Current Knowledge ◽  
Therapy Resistance ◽  
Cancer Associated Fibroblasts ◽  
Metastatic Progression ◽  
Normal Prostate ◽  
Prostate Tumorigenesis

Tumors strongly depend on their surrounding tumor microenvironment (TME) for growth and progression, since stromal elements are required to generate the optimal conditions for cancer cell proliferation, invasion, and possibly metastasis. Prostate cancer (PCa), though easily curable during primary stages, represents a clinical challenge in advanced stages because of the acquisition of resistance to anti-cancer treatments, especially androgen-deprivation therapies (ADT), which possibly lead to uncurable metastases such as those affecting the bone. An increasing number of studies is giving evidence that prostate TME components, especially cancer-associated fibroblasts (CAFs), which are the most abundant cell type, play a causal role in PCa since the very early disease stages, influencing therapy resistance and metastatic progression. This is highlighted by the prognostic value of the analysis of stromal markers, which may predict disease recurrence and metastasis. However, further investigations on the molecular mechanisms of tumor–stroma interactions are still needed to develop novel therapeutic approaches targeting stromal components. In this review, we report the current knowledge of the characteristics and functions of the stroma in prostate tumorigenesis, including relevant discussion of normal prostate homeostasis, chronic inflammatory conditions, pre-neoplastic lesions, and primary and metastatic tumors. Specifically, we focus on the role of CAFs, to point out their prognostic and therapeutic potential in PCa.

The role of WNT10B in normal prostate gland development and prostate cancer

The Prostate ◽  
2019 ◽  
Vol 79 (14) ◽  
pp. 1692-1704 ◽  
Author(s):  
Ikenna Madueke ◽  
Wen‐Yang Hu ◽  
Danping Hu ◽  
Steven M. Swanson ◽  
Donald Vander Griend ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Prostate Gland ◽  
Normal Prostate ◽  
Gland Development

miR-1825 Accelerates Cell Proliferation and Inhibits Cell Apoptosis of Prostate Cancer via Targeting Suppressor of Cancer Cell Invasion

2021 ◽  
Vol 11 (5) ◽  
pp. 820-831
Author(s):  
Jun-Chao Bai ◽  
Guang-Yi Huang
Keyword(s):  
Prostate Cancer ◽  
Cell Proliferation ◽  
Cancer Cell ◽  
Cell Invasion ◽  
Cell Apoptosis ◽  
Luciferase Reporter ◽  
Tunel Staining ◽  
Cancer Cell Invasion ◽  
Normal Prostate

Prostate cancer (PC) is one major carcinoma threat to the health of males. microRNAs (miRNAs) are short non-coding transcripts with about 23 nt in length. Booming evidence has verified the various roles of miRNAs in human tumors. miR-1825 was once demonstrated to be highly expressed in PC, but the potential role of miR-1825 in PC has never been clarified yet. This work aimed to explore the function of miR-1825 and reveal the underlying modulation mechanism in PC. First, miR-1825 was detected to be elevated in PC cells compared with normal prostate cells, as proved by RT-qPCR. After miR-1825 expression was inhibited, cell proliferation was hindered and cell apoptosis was promoted, which was observed by CCK8, colony formation, TUNEL staining and western blot assays. Bioinformatics tools discovered the targeting of suppressor of cancer cell invasion (SCAI) by miR-1825, which was further confirmed by luciferase reporter assay. Then the suppression of miR-1825 on SCAI protein expression was verified by western blotting. Eventually, rescue assays were implemented and affirmed the miR-1825/SCAI axis in PC cells. In conclusion, our present research disclosed the oncogenic role of miR-1825 and the miR-1825/SCAI pathway in PC. These findings gave new clues for the therapy of PC.

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 Dach1-Variant 4 Plays an Oncogenic Role and Promotes Radioresistance in Prostate Cancer

2021 ◽  
Author(s):  
Ilenia Giordani ◽  
Carlo M. Scornajenghi ◽  
Francesco Marampon ◽  
Antonella Stoppacciaro ◽  
Silvia Di Agostino ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Western Blot ◽  
Functional Role ◽  
Nuclear Staining ◽  
Western Blots ◽  
Normal Prostate ◽  
Mesenchymal Transition ◽  
Splicing Variants ◽  
Pc3 Cells

Abstract Background: Human Dachshund homologue 1 (DACH1) is involved in carcinogenesis with opposite roles reported in different tumor types. Four alternatively spliced transcripts encoding different DACH1 isoforms were described but their specific role in human cancers is still unknown. Prostate cancer (PCa) is a heterogeneous disease with a very wide variability, so there is yet a relevant need to find new diagnostic and therapeutic biomarkers to make a safe clinical evaluation. It is well known that the differential expression of protein isoforms can induce distinct transcriptional programs with opposing effects on tumor progression and therapy. Thus, in this study we aimed to correlate the functional role of DACH1 with its splicing variants expression in PCa.Methods: The expression and functional role of DACH1 splicing variants in PCa were investigated using tumor (PC3) and normal (RWPE-1) cell lines, patient biopsies and TCGA dataset. Flow-cytometry, western blots and RT-qPCR were used for in vitro molecular characterization; invasion, adhesion, clonogenic assays and cell cycle analysis for functional characterization. Immunohystochemistry and western blot were performed on human PCa biopsies.Results: RT-qPCR and Western Blot revealed that DACH1-positive PC3 cells predominantly expressed DACH1 variant 4 (DACH1-v4), whereas RWPE-1 cells mostly expressed DACH1 variant 3. Stable DACH1-v4 overexpression enhanced the transformed phenotype of PC3 cells by inducing proliferation, colony formation, invasion ability, epithelial to mesenchymal transition. Given its intrinsic radioresistance, PCa frequently recurs after radiotherapy. Of note, DACH1-v4-overexpressing PC3 cells displayed higher radioresistant behavior. Overexpression of DACH1-v4 also transformed RWPE-1 cells to oncogenic phenotype, suggesting a pro-oncogenic role for this specific isoform. PCa biopsies analysis showed DACH1 nuclear staining enhanced throughout the increase of the tumor grade. Remarkably, tumor glands were found to express a long DACH1 variant, while normal prostate tissue expressed the short DACH1 isoform, in line with data from TCGA-PRAD analysis and our data in RWPE-1 cells. Conclusions: Our findings highlight the oncogenic role of DACH1-v4 in PCa and suggest that the longer DACH1 variants could be associated to pro-tumor function, while the shortest DACH1 variant would perform tumor suppression. The expression of specific DACH1 isoforms could represent a novel diagnostic/prognostic marker in PCa.

Biological role of cytoplasmic transducin beta like related protein 1-induced proliferation and tumorigenicity in prostate cancer

2018 ◽  
Vol 6 (3) ◽  
pp. 223-235
Author(s):  
Shu-Peng Zheng ◽  
Xiang Feng
Keyword(s):  
Prostate Cancer ◽  
Clinical Stage ◽  
Immunohistochemical Analysis ◽  
Related Protein ◽  
Normal Prostate ◽  
Tissue Samples ◽  
Prostate Cell

Androgen receptor mediated transcription and function in prostate cancer and critical for prostate cell growth and gland differentiation. Transducin beta like related protein 1 (TBLR1) primarily localizes in the nucleus in benign prostate tissue and is significantly reduced in prostate cancer. The objective of this study is investigated the role of cytoplasmic TBLR1in prostate cancer. Real-time PCR, Western blotting and immunocytochemistry were used to evaluate Transducin beta like related protein 1 (TBLR1) expression in prostate cancer cell lines and normal prostate cells, tissue samples and adjacent nontumor tissues, and in 142 paraffin-embedded specimens. Immunohistochemical analysis revealed high expression of TBLR1 in 89 of 214 paraffin-embedded archival prostate cancer. The expression level of TBLR1 was significantly increased in prostate cancer both in vivo and in vitro and correlated with clinical stage (P<0.05) and metastasis (P<0.001). Over all the study showed that the TBLR1 plays a key role in the development of prostate cancer cells and TBLR1 may be prognostic marker and a potential therapeutic target in the treatment human prostate cancer.

scholarly journals Circular RNA-DPP4 serves an oncogenic role in prostate cancer progression through regulating miR-195/cyclin D1 axis

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Deping Yang ◽  
Bo Yang ◽  
Yanjun Zhu ◽  
Qianlin Xia ◽  
Yan Zhang ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Cycle ◽  
Tumor Growth ◽  
Cyclin D1 ◽  
Microarray Analysis ◽  
Cell Cycle Progression ◽  
Normal Prostate ◽  
Cycle Progression

Abstract Background Recently, more and more studies have highlighted the critical regulatory roles of circular RNAs (circRNAs), a class of non-coding RNAs, in the progression of many human cancers, including prostate cancer (PCa). circRNA microarray analysis was performed to identify circRNAs that are differentially expressed in PCa tissues. Methods 104 pairs of PCa tissues and matched adjacent normal prostate tissues (at least 2 cm distal to the tumor margin) were obtained. circRNA microarray analysis was performed on four pairs of PCa tissues and matched adjacent normal prostate tissues to investigate the potential involvement of circRNAs in PCa. Flow cytometric analysis was performed to investigate whether the effect of circDPP4 on PCa cell proliferation was associated with the alteration in cell cycle progression. The role of circDPP4 in PCa tumor growth was further explored in vivo. Results We found that circDPP4 was overexpressed in PCa tissues and cell lines, and its expression was closely associated with Gleason score and clinical stage of PCa patients. In vitro loss- and gain-of-function experiments demonstrated that circDPP4 knockdown inhibited, whereas circDPP4 overexpression promoted the proliferation, migration, invasion and cell cycle progression of PCa cells. Knockdown of circDPP4 also suppressed PCa tumor growth in vivo. We further found that circDPP4 functioned as a competing endogenous RNA (ceRNA) for miR-195 in PCa cells, and miR-195 negatively regulated the expression of oncogenic cyclin D1. Rescue experiments suggested that restoration of miR-195 blocked the oncogenic role of circDPP4 in PCa cells. Conclusions Taken together, our findings revealed a novel regulatory mechanism between circDPP4 and miR-195/cyclin D1 axis, and offered novel strategies for the treatment of PCa.

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