Modulation of Phospho Tensin Homolog (PTEN) in Cancer Cells and Lipid Peroxides in Peripheral Blood Mononuclear Cells (PBMCs) Following Exposure to Flavonoids


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William Boadi1,William Boadi1,Alekzander Garcia1,Elbert Myles1
1Tennessee State University

Abstract

Background

Plant flavonoids have been shown to offer more protective health benefits against oxidative deoxyribonucleic acid (DNA) damages caused by g-ray radiation, UV irradiation, chemicals, and endogenous oxidative stress. The above compounds have been shown to be capable of modulating the activity of enzymes, and affect the behavior of many cell systems. While these may account for the anti-mutagenic activities of flavonoids in experimental systems, relatively little is known about the mechanisms of the modulation of PTEN activity in cancer cells and the levels of lipid peroxides in peripheral blood mononuclear cells (PMBCs). The objectives of this study was to investigate the effects of three flavonoids: quercetin, kaempferol and genistein on the expression levels of both phospho- and total-PTEN in breast cancer (BT-549), lung cancer (A-549) and human preadipocytes (3T3-L1 which was used as controls). Furthermore, the effects of the flavonoids on lipid peroxides in PMBCs were investigated. Cells were seeded and were exposed to each of the flavonoid at concentrations of 0, 5, 10, 15, 20 and 25 ┬ÁM and the phosphorylation of PTEN at Ser380, total PTEN levels, and lipid peroxides (i.e., malonaldehyde (MDA before and after the oxidative stress)) levels were measured. The results indicate the flavonoids increased both phospho-PTEN- and total-PTEN levels increased in a dose-dependent manner. The effect of quercetin was more pronounced followed by genistein and kaempferol. Exposure of PMBCs cells to the various flavonoids at the different concentrations lowered the MDA levels compared to their respective controls. Levels of MDA in quercetin treated samples were lower compared to kaempferol and genistein. The findings suggest that the flavonoids play an important role in controlling oxidative stress in cells.