Methylated urolithin A, the modified ellagitannin-derived metabolite, suppresses cell viability of DU145 human prostate cancer cells via targeting miR-21

2016 ◽  
Vol 97 ◽  
pp. 375-384 ◽  
Author(s):  
Benhong Zhou ◽  
Jing Wang ◽  
Guohua Zheng ◽  
Zhenpeng Qiu
Keyword(s):  
Prostate Cancer ◽  
Cell Viability ◽  
Cancer Cells ◽  
Human Prostate ◽  
Human Prostate Cancer ◽  
Prostate Cancer Cells ◽  
Urolithin A

Phytoestrogen modulation of bone-related cytokines and its impact on cell viability in human prostate cancer cells

Life Sciences ◽  
2009 ◽  
Vol 85 (11-12) ◽  
pp. 421-430 ◽  
Author(s):  
V. Alonso ◽  
F.C. Pérez-Martínez ◽  
F.J. Calahorra ◽  
P. Esbrit
Keyword(s):  
Prostate Cancer ◽  
Cell Viability ◽  
Cancer Cells ◽  
Human Prostate ◽  
Human Prostate Cancer ◽  
Prostate Cancer Cells

Mechanisms of resveratrol-induced changes in [Ca2+]iand cell viability in PC3 human prostate cancer cells

2013 ◽  
Vol 33 (5) ◽  
pp. 298-303 ◽  
Author(s):  
Hong-Tai Chang ◽  
Chiang-Ting Chou ◽  
I-Li Chen ◽  
Wei-Zhe Liang ◽  
Daih-Huang Kuo ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Viability ◽  
Cancer Cells ◽  
Human Prostate ◽  
Human Prostate Cancer ◽  
Prostate Cancer Cells ◽  
Induced Changes

Ca2+ movement and cytotoxicity induced by the pyrethroid pesticide bifenthrin in human prostate cancer cells

2019 ◽  
Vol 38 (10) ◽  
pp. 1145-1154 ◽  
Author(s):  
J-M Chien ◽  
W-Z Liang ◽  
W-C Liao ◽  
C-C Kuo ◽  
C-T Chou ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Endoplasmic Reticulum ◽  
Cell Viability ◽  
Cancer Cells ◽  
Water Soluble ◽  
Human Prostate ◽  
Human Prostate Cancer ◽  
Prostate Cancer Cells ◽  
Fura 2 ◽  
Pyrethroid Pesticide

Bifenthrin, a commonly used pyrethroid pesticide, evokes various toxicological effects in different models. However, the effect of bifenthrin on cytosolic-free Ca2+ level ([Ca2+] i) and cytotoxicity in human prostate cancer cells is unclear. This study examined whether bifenthrin altered Ca2+ homeostasis and cell viability in PC3 human prostate cancer cells. [Ca2+] i in suspended cells were measured using the fluorescent Ca2+-sensitive dye fura-2. Cell viability was examined by 4-[3-[4-lodophenyl]-2-4(4-nitrophenyl)-2H-5-tetrazolio-1,3-benzene disulfonate] water soluble tetrazolium-1 assay. Bifenthrin (100–400 μM) concentration-dependently induced [Ca2+] i rises. Ca2+ removal reduced the signal by approximately 30%. In Ca2+-free medium, treatment with the endoplasmic reticulum Ca2+ pump inhibitor 2,5-di-tert-butylhydroquinone (BHQ) abolished bifenthrin-evoked [Ca2+] i rises. Conversely, treatment with bifenthrin abolished BHQ-evoked [Ca2+] i rises. Inhibition of phospholipase C (PLC) with U73122 significantly inhibited bifenthrin-induced [Ca2+] i rises. Mn2+ has been shown to enter cells through similar mechanisms as Ca2+ but quenches fura-2 fluorescence at all excitation wavelengths. Bifenthrin (400 μM)-induced Mn2+ influx implicates that Ca2+ entry occurred. Bifenthrin-induced Ca2+ entry was inhibited by 30% by protein kinase C (PKC) activator (phorbol 12-myristate 13 acetate) and inhibitor (GF109203X) and three inhibitors of store-operated Ca2+ channels: nifedipine, econazole, and SKF96365. Bifenthrin at 175–275 μM decreased cell viability, which was not reversed by pretreatment with the Ca2+ chelator 1,2-bis(2-aminophenoxy) ethane- N, N, N′, N′-tetra acetic acid-acetoxymethyl ester. Together, in PC3 cells, bifenthrin-induced [Ca2+] i rises by evoking PLC-dependent Ca2+ release from the endoplasmic reticulum and Ca2+ entry via PKC-sensitive store-operated Ca2+ entry. Bifenthrin also caused Ca2+-independent cell death.

scholarly journals Heme Oxygenase-1 Inhibition Sensitizes Human Prostate Cancer Cells towards Glucose Deprivation and Metformin-Mediated Cell Death

2019 ◽  
Vol 20 (10) ◽  
pp. 2593 ◽  
Author(s):  
Marco Raffaele ◽  
Valeria Pittalà ◽  
Veronica Zingales ◽  
Ignazio Barbagallo ◽  
Loredana Salerno ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Death ◽  
Cell Viability ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Heme Oxygenase ◽  
Glucose Concentration ◽  
Human Prostate ◽  
Human Prostate Cancer ◽  
Prostate Cancer Cells

High levels of heme oxygenase (HO)-1 have been frequently reported in different human cancers, playing a major role in drug resistance and regulation of cancer cell redox homeostasis. Metformin (MET), a drug widely used for type 2 diabetes, has recently gained interest for treating several cancers. Recent studies indicated that the anti-proliferative effects of metformin in cancer cells are highly dependent on glucose concentration. The present work was directed to determine whether use of a specific inhibitor of HO-1 activity, alone or in combination with metformin, affected metastatic prostate cancer cell viability under different concentrations of glucose. MTT assay and the xCELLigence system were used to evaluate cell viability and cell proliferation in DU145 human prostate cancer cells. Cell apoptosis and reactive oxygen species were analyzed by flow cytometry. The activity of HO-1 was inhibited using a selective imidazole-based inhibitor; genes associated with antioxidant systems and cell death were evaluated by qRT-PCR. Our study demonstrates that metformin suppressed prostate cancer growth in vitro and increased oxidative stress. Disrupting the antioxidant HO-1 activity, especially under low glucose concentration, could be an attractive approach to potentiate metformin antineoplastic effects and could provide a biochemical basis for developing HO-1-targeting drugs against solid tumors.

Osteoblast-derived factors increased metastatic potential in human prostate cancer cells

2016 ◽  
Author(s):  
Terese Karlsson ◽  
Reshma Sundar ◽  
Anders Widmark ◽  
Marene Landstrom ◽  
Emma Persson
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Metastatic Potential ◽  
Human Prostate ◽  
Human Prostate Cancer ◽  
Prostate Cancer Cells
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