scholarly journals  -Mangostin, a xanthone from mangosteen fruit, promotes cell cycle arrest in prostate cancer and decreases xenograft tumor growth

2011 ◽  
Vol 33 (2) ◽  
pp. 413-419 ◽  
Author(s):  
J. J. Johnson ◽  
S. M. Petiwala ◽  
D. N. Syed ◽  
J. T. Rasmussen ◽  
V. M. Adhami ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Cycle ◽  
Tumor Growth ◽  
Cell Cycle Arrest ◽  
Xenograft Tumor ◽  
Cycle Arrest ◽  
Xenograft Tumor Growth

scholarly journals Mechanism of Growth Inhibition of Prostate Cancer Xenografts by Valproic Acid

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Abhinav Sidana ◽  
Muwen Wang ◽  
Shabana Shabbeer ◽  
Wasim H. Chowdhury ◽  
George Netto ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Cycle ◽  
Valproic Acid ◽  
Tumor Growth ◽  
Growth Inhibition ◽  
Cell Cycle Arrest ◽  
Cycle Arrest ◽  
Angiogenic Effect

Valproic Acid (VPA), a histone deacetylase inhibitor, has been demonstrated to cause a marked decrease in proliferation of prostate cancer (PCa) cellsin vitroand a significant reduction in tumor volumein vivo. The goal of this study is to better understand the VPA-induced growth inhibitionin vivo, by studying expression of various markers in PCa xenografts.Methods. Forin vitroexperiments, PCa cells were treated with 0, 0.6, and 1.2 mM VPA for 14 days. Forin vivomodels, experimental animals received 0.4% VPA in drinking water for 35 days. Tissue microarray was generated using cell pellets and excised xenografts.Results. VPA treatment causes cell cycle arrest in PCa cellsin vivo, as determined by increase in p21 and p27 and decrease in cyclin D1 expression. Increased expression of cytokeratin18 was also seen in xenografts. LNCaP xenografts in treated animals had reduced androgen receptor (AR) expression. While decreased proliferation was foundin vitro, increase in apoptosis was found to be the reason for decreased tumor growthin vivo. Also, an anti-angiogenic effect was observed after VPA treatment.Conclusion. VPA inhibits tumor growth by multiple mechanisms including cell cycle arrest, induction of differentiation, and inhibition of growth of tumor vasculature.

scholarly journals APE1/Ref-1 redox-specific inhibition decreases survivin protein levels and induces cell cycle arrest in prostate cancer cells

Oncotarget ◽  
2017 ◽  
Vol 9 (13) ◽  
pp. 10962-10977 ◽  
Author(s):  
David W. McIlwain ◽  
Melissa L. Fishel ◽  
Alexander Boos ◽  
Mark R. Kelley ◽  
Travis J. Jerde
Keyword(s):  
Prostate Cancer ◽  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Specific Inhibition ◽  
Prostate Cancer Cells ◽  
Protein Levels ◽  
Survivin Protein ◽  
Cycle Arrest

scholarly journals Effect of Piceatannol on Cell Cycle Progression in Prostate Cancer Cells (P05-005-19)

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Larissa Kido ◽  
Eun-Ryeong Hahm ◽  
Valeria Cagnon ◽  
Mário Maróstica ◽  
Shivendra Singh
Keyword(s):  
Prostate Cancer ◽  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Cell Lines ◽  
Cell Cycle Progression ◽  
Cell Cycle Distribution ◽  
Mutant P53 ◽  
Wild Type ◽  
Cycle Progression ◽  
Cycle Arrest

Abstract Objectives Piceatannol (PIC) is a polyphenolic and resveratrol analog that is found in many vegetables consumed by humans. Like resveratrol, PIC has beneficial effects on health due to its anti-inflammatory, anti-oxidative and anti-proliferative features. However, the molecular targets of PIC in prostate cancer (PCa), which is the second most common cancer in men worldwide, are still poorly understood. Preventing cancer through dietary sources is a promising strategy to control diseases. Therefore, the aim of present study was to investigate the molecular mechanistic of actions of PIC in PCa cell lines with different genetic background common to human prostate cancer. Methods Human PCa cell lines (PC-3, 22Rv1, LNCaP, and VCaP) were treated with different doses of PIC (5–40 µM) and used for cell viability assay, measurement of total free fatty acids (FFA) and lactate, and cell cycle distribution. Results PIC treatment dose- and time-dependently reduced viability in PC-3 (androgen-independent, PTEN null, p53 null) and VCaP cells (androgen-responsive, wild-type PTEN, mutant p53). Because metabolic alterations, such as increased glucose and lipid metabolism are implicated in pathogenesis of in PCa, we tested if PIC could affect these pathways. Results from lactate and total free fatty acid assays in VCaP, 22Rv1 (castration-resistant, wild-type PTEN, mutant p53), and LNCaP (androgen-responsive, PTEN null, wild-type p53) revealed no effect of PIC on these metabolisms. However, PIC treatment delayed cell cycle progression in G0/G1 phase concomitant with the induction of apoptosis in both LNCaP and 22Rv1 cells, suggesting that growth inhibitory effect of PIC in PCa is associated with cell cycle arrest and apoptotic cell death at least LNCaP and 22Rv1 cells. Conclusions While PIC treatment does not alter lipid or glucose metabolism, cell cycle arrest and apoptosis induction are likely important in anti-cancer effects of PIC. Funding Sources São Paulo Research Foundation (2018/09793-7).

scholarly journals Lipophilized Epigallocatechin Gallate Derivative Exerts Anti-Proliferation Efficacy through Induction of Cell Cycle Arrest and Apoptosis on DU145 Human Prostate Cancer Cells

Nutrients ◽  
2019 ◽  
Vol 12 (1) ◽  
pp. 92 ◽  
Author(s):  
Jun Chen ◽  
Linli Zhang ◽  
Changhong Li ◽  
Ruochen Chen ◽  
Chengmei Liu ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Epigallocatechin Gallate ◽  
Human Prostate ◽  
Enzymatic Esterification ◽  
Cytochrome C Release ◽  
Cycle Arrest ◽  
13C Nuclear Magnetic Resonance ◽  
Du145 Cells

Epigallocatechin gallate (EGCG) is the predominant tea polyphenol and it exhibits a hydrophilic character. The lipophilized EGCG derivative (LEGCG) was synthesized by enzymatic esterification of EGCG with lauric acid to enhance its bioactivity. The tetralauroyl EGCG was confirmed by high-performance liquid chromatography-tandem mass spectrometry and further identified as 3′, 5′, 3″, 5″-4-O-lauroyl EGCG by 1H and 13C nuclear magnetic resonance. The anti-proliferation effect of LEGCG on DU145 human prostate carcinoma cells was evaluated by MTT assay. In addition, the underlying molecular mechanism by which LEGCG exerts anti-proliferation efficacy was elucidated by flow cytometry and immunoblot analysis. Results suggested that LEGCG exhibited a dose-dependent anti-proliferation effect on DU145 cells by G0/G1 phase arrest and induction of apoptosis. LEGCG induced cell cycle arrest via p53/p21 activation, which down-regulated the cyclin D1 and CDK4 expression. In addition, LEGCG induced apoptosis by increasing the Bax/Bcl-2 ratio, the cytochrome c release, and the caspases cleavage on DU145 cells. The results provide theoretical support to prevent prostate cancer with LEGCG.

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