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dc.contributor.authorBenazic S.-
dc.contributor.authorSilconi Z.-
dc.contributor.authorJevtovic A.-
dc.contributor.authorJurisevic M.-
dc.contributor.authorMilovanovic, Jelena-
dc.contributor.authorMijajlovic M.-
dc.contributor.authorNikolic, Milos-
dc.contributor.authorKanjevac, Tatjana-
dc.contributor.authorPotočňák I.-
dc.contributor.authorSamoľová, Erika-
dc.contributor.authorRatković, Zoran-
dc.contributor.authorRadic G.-
dc.contributor.authorMilovanovic, Marija-
dc.contributor.authorPantic, Jelena-
dc.contributor.authorArsenijevic, Nebojsa-
dc.contributor.authorRadosavljevic, Gordana-
dc.description.abstract© 2020 Newlands Press. Aim: We investigated the antitumor effects of zinc(II) complex with S-propyl thiosalicylic acid [Zn(S-pr-thiosal)2] in 4T1 murine breast cancer model. Results: The Zn(S-pr-thiosal)2 complex reduced primary tumor growth in vivo and induced tumor cell apoptosis. The Zn(S-pr-thiosal)2 complex disrupted the balance between pro- and antiapoptotic Bcl-2 family members in 4T1 cells and induced G1/S cell cycle arrest. The Zn(S-pr-thiosal)2 complex increased the percentage of p16, p21 and p27 positive 4T1 cells. There was a significantly decrease in expression of STAT3 and its targets c-Myc and cyclin D3 in 4T1 cells treated with the Zn(S-pr-thiosal)2 complex thus contributing to G1/S cell cycle arrest and/or apoptosis. Conclusion: Our data suggest that the Zn(S-pr-thiosal)2 complex restricted tumor growth through induction of mitochondrial-driven apoptosis and suppression of cell cycle progression.-
dc.sourceFuture Medicinal Chemistry-
dc.titleThe Zn(S-pr-thiosal)<inf>2</inf> complex attenuates murine breast cancer growth by inducing apoptosis and G1/S cell cycle arrest-
Appears in Collections:Faculty of Medical Sciences, Kragujevac
Faculty of Science, Kragujevac

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