High Density Lipoproteins Inhibit Oxidative Stress-Induced Prostate Cancer Cell Proliferation

Abstract Recent evidence suggests that oxidative stress can play a role in the pathogenesis and the progression of prostate cancer (PCa). Reactive oxygen species (ROS) generation is higher in PCa cells compared to normal prostate epithelial cells and this increase is proportional to the aggressivene...

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Autores principales:	Massimiliano Ruscica, Margherita Botta, Nicola Ferri, Eleonora Giorgio, Chiara Macchi, Guido Franceschini, Paolo Magni, Laura Calabresi, Monica Gomaraschi
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2018
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/236f961aaeed4316833c7b6131b30204
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spelling	oai:doaj.org-article:236f961aaeed4316833c7b6131b302042021-12-02T15:08:02ZHigh Density Lipoproteins Inhibit Oxidative Stress-Induced Prostate Cancer Cell Proliferation10.1038/s41598-018-19568-82045-2322https://doaj.org/article/236f961aaeed4316833c7b6131b302042018-02-01T00:00:00Zhttps://doi.org/10.1038/s41598-018-19568-8https://doaj.org/toc/2045-2322Abstract Recent evidence suggests that oxidative stress can play a role in the pathogenesis and the progression of prostate cancer (PCa). Reactive oxygen species (ROS) generation is higher in PCa cells compared to normal prostate epithelial cells and this increase is proportional to the aggressiveness of the phenotype. Since high density lipoproteins (HDL) are known to exert antioxidant activities, their ability to reduce ROS levels and the consequent impact on cell proliferation was tested in normal and PCa cell lines. HDL significantly reduced basal and H2O2-induced oxidative stress in normal, androgen receptor (AR)-positive and AR-null PCa cell lines. AR, scavenger receptor BI and ATP binding cassette G1 transporter were not involved. In addition, HDL completely blunted H2O2-induced increase of cell proliferation, through their capacity to prevent the H2O2-induced shift of cell cycle distribution from G0/G1 towards G2/M phase. Synthetic HDL, made of the two main components of plasma-derived HDL (apoA-I and phosphatidylcholine) and which are under clinical development as anti-atherosclerotic agents, retained the ability of HDL to inhibit ROS production in PCa cells. Collectively, HDL antioxidant activity limits cell proliferation induced by ROS in AR-positive and AR-null PCa cell lines, thus supporting a possible role of HDL against PCa progression.Massimiliano RuscicaMargherita BottaNicola FerriEleonora GiorgioChiara MacchiGuido FranceschiniPaolo MagniLaura CalabresiMonica GomaraschiNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 8, Iss 1, Pp 1-12 (2018)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Massimiliano Ruscica Margherita Botta Nicola Ferri Eleonora Giorgio Chiara Macchi Guido Franceschini Paolo Magni Laura Calabresi Monica Gomaraschi High Density Lipoproteins Inhibit Oxidative Stress-Induced Prostate Cancer Cell Proliferation
description	Abstract Recent evidence suggests that oxidative stress can play a role in the pathogenesis and the progression of prostate cancer (PCa). Reactive oxygen species (ROS) generation is higher in PCa cells compared to normal prostate epithelial cells and this increase is proportional to the aggressiveness of the phenotype. Since high density lipoproteins (HDL) are known to exert antioxidant activities, their ability to reduce ROS levels and the consequent impact on cell proliferation was tested in normal and PCa cell lines. HDL significantly reduced basal and H2O2-induced oxidative stress in normal, androgen receptor (AR)-positive and AR-null PCa cell lines. AR, scavenger receptor BI and ATP binding cassette G1 transporter were not involved. In addition, HDL completely blunted H2O2-induced increase of cell proliferation, through their capacity to prevent the H2O2-induced shift of cell cycle distribution from G0/G1 towards G2/M phase. Synthetic HDL, made of the two main components of plasma-derived HDL (apoA-I and phosphatidylcholine) and which are under clinical development as anti-atherosclerotic agents, retained the ability of HDL to inhibit ROS production in PCa cells. Collectively, HDL antioxidant activity limits cell proliferation induced by ROS in AR-positive and AR-null PCa cell lines, thus supporting a possible role of HDL against PCa progression.
format	article
author	Massimiliano Ruscica Margherita Botta Nicola Ferri Eleonora Giorgio Chiara Macchi Guido Franceschini Paolo Magni Laura Calabresi Monica Gomaraschi
author_facet	Massimiliano Ruscica Margherita Botta Nicola Ferri Eleonora Giorgio Chiara Macchi Guido Franceschini Paolo Magni Laura Calabresi Monica Gomaraschi
author_sort	Massimiliano Ruscica
title	High Density Lipoproteins Inhibit Oxidative Stress-Induced Prostate Cancer Cell Proliferation
title_short	High Density Lipoproteins Inhibit Oxidative Stress-Induced Prostate Cancer Cell Proliferation
title_full	High Density Lipoproteins Inhibit Oxidative Stress-Induced Prostate Cancer Cell Proliferation
title_fullStr	High Density Lipoproteins Inhibit Oxidative Stress-Induced Prostate Cancer Cell Proliferation
title_full_unstemmed	High Density Lipoproteins Inhibit Oxidative Stress-Induced Prostate Cancer Cell Proliferation
title_sort	high density lipoproteins inhibit oxidative stress-induced prostate cancer cell proliferation
publisher	Nature Portfolio
publishDate	2018
url	https://doaj.org/article/236f961aaeed4316833c7b6131b30204
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High Density Lipoproteins Inhibit Oxidative Stress-Induced Prostate Cancer Cell Proliferation

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