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• W3012650168 endingPage "108638" @default.
• W3012650168 startingPage "108638" @default.
• W3012650168 abstract "Cholest-4-ene-3,6-dione (KS) is a cholesterol oxidation product which exhibits anti-proliferative activity. However, its precise mechanism of action remains unknown. In this study, the effects of KS on AKR1C3 inhibition and anti-proliferative activities were investigated in the hormone-dependent MCF-7 breast cancer cells. We identified that KS arrested the enzymatic conversion of estrone to 17-β estradiol, by inhibiting AKR1C3 in intact MCF-7 cells. The anti-proliferative effects of KS were evaluated by MTT assay, acridine orange and ethidium bromide dual staining, cell cycle analysis and Western blotting. KS arrested the cell cycle progression in the G1 phase with a concomitant increase of the Sub-G0 population to increase in concentration and time. It also enhanced the p53 and NFkB expression and induced caspase-12, 9 and 3 processing and down-regulated the Bcl-2 expression. Molecular docking studies performed to understand the inhibition mechanism of KS on AKR1C3 revealed that KS occupied the binding region of AKR1C3 with almost similar orientation as indomethacin (IM), thereby acting as an antagonistic agent for AKR1C3. Based on the results it is identified that KS induces inhibition of AKR1C3 and cell death in MCF-7 cells. These results indicate that KS can be used as a molecular scaffold for further development of novel small-molecules with better specificity towards AKR1C3." @default.
• W3012650168 created "2020-03-27" @default.
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• W3012650168 date "2020-07-01" @default.
• W3012650168 modified "2023-10-14" @default.
• W3012650168 title "Type 5 17-hydroxysteroid dehydrogenase/prostaglandin F synthase (AKR1C3) inhibition and potential anti-proliferative activity of cholest-4-ene-3,6-dione in MCF-7 breast cancer cells" @default.
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• W3012650168 doi "https://doi.org/10.1016/j.steroids.2020.108638" @default.
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