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High Density Lipoproteins Inhibit Oxidative Stress-Induced Prostate Cancer Cell Proliferation
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Journal Article
High Density Lipoproteins Inhibit Oxidative Stress-Induced Prostate Cancer Cell Proliferation
2018
Overview
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 H
2
O
2
-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 H
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O
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-induced increase of cell proliferation, through their capacity to prevent the H
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-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.
Publisher
Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio
Subject
/ 13/89
/ 631/80
/ 82/29
/ 96/34
/ Antioxidants - chemical synthesis
/ Apolipoprotein A-I - chemical synthesis
/ Apolipoprotein A-I - pharmacology
/ Cell Proliferation - drug effects
/ Humanities and Social Sciences
/ Humans
/ Hydrogen Peroxide - metabolism
/ Lecithin
/ Lipoproteins, HDL - metabolism
/ Male
/ Oxidative Stress - drug effects
/ Phosphatidylcholines - chemical synthesis
/ Phosphatidylcholines - pharmacology
/ Prostatic Neoplasms - pathology
/ RNA, Small Interfering - genetics
/ Science
