scholarly journals Roles of Cell Cycle Regulators [p53, Cathepsin-D and Bax] in Prognostic Determination of Prostate Cancer and Benign Prostatic Hyperplasia

2013 ◽  
Author(s):  
Ogundele M Olalekan Ajonijebu D Chris
Keyword(s):  
Prostate Cancer ◽  
Cell Cycle ◽  
Benign Prostatic Hyperplasia ◽  
Cathepsin D ◽  
Prostatic Hyperplasia ◽  
Cell Cycle Regulators

scholarly journals Synthesis of novel andostane-N-cyclohexyl-17-carboxamides, and their effect on the 5α-reductase isoform 2, the androgen receptor, and androgen-dependent glands

2021 ◽  
Author(s):  
Juan Carlos Lopez-Lezama ◽  
Marisa Cabeza ◽  
Yvonne Heuze ◽  
Araceli Sánchez ◽  
José L. Rojas ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Biological Activity ◽  
Androgen Receptor ◽  
Benign Prostatic Hyperplasia ◽  
Seminal Vesicles ◽  
Prostatic Hyperplasia ◽  
New Drugs ◽  
Binding Assays ◽  
Competitive Binding Assays

Background: Benign Prostatic Hyperplasia (BPH), and Prostate Cancer (PCa) are androgen-dependent diseases. PCa is associated with excessive signalling of the androgen receptor (AR) due to the binding of 5α-DHT and T. BPH is related to high levels of 5α-dihydrotestosterone (5α-DHT), biosynthesized from testosterone (T) by 5α-reductase (5RD5A). The inhibition of 5RD5A and the blockage of AR are targets for their treatment. In this study, the synthesis and determination of biological activity of the new N-cyclohexyl-3β-hydroxyandrosta-5,16-diene-17-carboxamide (6), N-cyclohexyl-3-oxoandrosta-4,6,16-triene-17-carboxamide (7), and N-cyclohexyl-3-oxoandrosta-4,16-diene-17-carboxamide (8) were carried out to find new drugs to improve these afflictions. Methods: The synthesis of 6 to 8 was confirmed by spectroscopic and spectrometric analyses. Competitive binding assays determined the affinity of 6 to 8 to the AR. The inhibitory activity of 5RD5A isoform 2 (5RD5A2) (IC50) was established by the conversion of [3H]-T to [3H]-5α-DHT and it was compared with finasteride (FIN). The pharmacological effect of 6 to 8 was determined on the weight of the prostate and seminal vesicles glands of castrated hamsters treated with T, and on the diameter size of their flank organs. Results: Compounds 7 and 8 bound lightly (ca. 15 %) to AR. Comparing to FIN (IC50 = 8.5 nM), 6 to 8 (IC50 = 0.169, 0.105 and 0.155 nM, respectively) showed higher potency as inhibitors of 5RD5A2. Compound 6 decreased the prostate and seminal vesicles weight, as well as the hamsters' diameter flank organs. However, 7 only decreased the diameter of flank organs. Surprisingly, 8 increased these pharmacological parameters. Conclusion: Androstane-17-caboxamide 6 is a 5RD5A2 inhibitor that reduces the weight of androgen-dependent glands such as the prostate, suggesting it could be a lead for new drugs to treat BPH and PCa.

468: Polymorphic CA Repeats in IGF-I Gene is a Common Genetic Modifier in the Etiology of Prostate Cancer and Benign Prostatic Hyperplasia

2004 ◽  
Vol 171 (4S) ◽  
pp. 125-125
Author(s):  
Lizhong Wang ◽  
Kazunari Sato ◽  
Norihiko Tsuchiya ◽  
Chikara Ohyama ◽  
Shigeru Satoh ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Benign Prostatic Hyperplasia ◽  
Genetic Modifier ◽  
Prostatic Hyperplasia ◽  
Igf I ◽  
I Gene

scholarly journals Light-controlled calcium signalling in prostate cancer and benign prostatic hyperplasia

2020 ◽  
Vol 6 (1) ◽  
Author(s):  
Vipin Sharma ◽  
Rita Rana ◽  
Ruma Baksi ◽  
Swapnil P. Borse ◽  
Manish Nivsarkar
Keyword(s):  
Prostate Cancer ◽  
Benign Prostatic Hyperplasia ◽  
Calcium Signalling ◽  
Prostatic Hyperplasia

scholarly journals The Etiology and Pathophysiology Genesis of Benign Prostatic Hyperplasia and Prostate Cancer: A New Perspective

Medicines ◽  
2021 ◽  
Vol 8 (6) ◽  
pp. 30
Author(s):  
Teow J. Phua
Keyword(s):  
Prostate Cancer ◽  
Benign Prostatic Hyperplasia ◽  
Cell Biology ◽  
Cancer Biology ◽  
Cost Savings ◽  
Prostatic Hyperplasia ◽  
Biological Processes ◽  
New Perspective ◽  
Prostatic Diseases

Background: The etiology of benign prostatic hyperplasia and prostate cancer are unknown, with ageing being the greatness risk factor. Methods: This new perspective evaluates the available interdisciplinary evidence regarding prostate ageing in terms of the cell biology of regulation and homeostasis, which could explain the timeline of evolutionary cancer biology as degenerative, inflammatory and neoplasm progressions in these multifactorial and heterogeneous prostatic diseases. Results: This prostate ageing degeneration hypothesis encompasses the testosterone-vascular-inflamm-ageing triad, along with the cell biology regulation of amyloidosis and autophagy within an evolutionary tumorigenesis microenvironment. Conclusions: An understanding of these biological processes of prostate ageing can provide potential strategies for early prevention and could contribute to maintaining quality of life for the ageing individual along with substantial medical cost savings.

Soluble CD44 molecules in serum of patients with prostate cancer and benign prostatic hyperplasia

1996 ◽  
Vol 32 (4) ◽  
pp. 627-630 ◽  
Author(s):  
K. Jung ◽  
M. Lein ◽  
S. Weiss ◽  
D. Schnorr ◽  
W. Henke ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Benign Prostatic Hyperplasia ◽  
Prostatic Hyperplasia ◽  
Soluble Cd44

scholarly journals The treatment effects of flaxseed-derived secoisolariciresinol diglycoside and its metabolite enterolactone on benign prostatic hyperplasia involve the G protein-coupled estrogen receptor 1

2016 ◽  
Vol 41 (12) ◽  
pp. 1303-1310 ◽  
Author(s):  
Guan-Yu Ren ◽  
Chun-Yang Chen ◽  
Wei-Guo Chen ◽  
Ya Huang ◽  
Li-Qiang Qin ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Estrogen Receptor ◽  
Benign Prostatic Hyperplasia ◽  
G Protein ◽  
Therapeutic Potential ◽  
Prostatic Hyperplasia ◽  
Docking Simulations ◽  
G Protein Coupled

Secoisolariciresinol diglucoside (SDG), a lignan extracted from flaxseed, has been shown to suppress benign prostatic hyperplasia (BPH). However, little is known about the mechanistic basis for its anti-BPH activity. The present study showed that enterolactone (ENL), the mammalian metabolite of SDG, shared the similar binding site of G1 on a new type of membranous estrogen receptor, G-protein-coupled estrogen eceptor 1 (GPER), by docking simulations method. ENL and G1 (the specific agonist of GPER) inhibited the proliferation of human prostate stromal cell line WPMY-1 as shown by MTT assay and arrested cell cycle at the G0/G1 phase, which was displayed by propidium iodide staining following flow cytometer examination. Silencing GPER by short interfering RNA attenuated the inhibitory effect of ENL on WPMY-1 cells. The therapeutic potential of SDG in the treatment of BPH was confirmed in a testosterone propionate-induced BPH rat model. SDG significantly reduced the enlargement of the rat prostate and the number of papillary projections of prostatic alveolus and thickness of the pseudostratified epithelial and stromal cells when comparing with the model group. Mechanistic studies showed that SDG and ENL increased the expression of GPER both in vitro and in vivo. Furthermore, ENL-induced cell cycle arrest may be mediated by the activation of GPER/ERK pathway and subsequent upregulation of p53 and p21 and downregulation of cyclin D1. This work, in tandem with previous studies, will enhance our knowledge regarding the mechanism(s) of dietary phytochemicals on BPH prevention and ultimately expand the scope of adopting alternative approaches in BPH treatment.

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