کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2583231 | 1130684 | 2013 | 11 صفحه PDF | دانلود رایگان |
The current work investigates the influence of novel dinuclear platinum(II) compounds of structure: Pt2(3-ethylpyridine)4(berenil)2 (Pt10) and Pt2(3-butylpyridine)4(berenil)2 (Pt11) on growth and viability of MDA-MB-231 and MCF-7 breast cancer cells as well as their putative mechanism of cytotoxicity. Evaluation of the cytotoxicity of Pt10 and Pt11 employing a MTT assay and inhibition of [3H]thymidine incorporation into DNA in both MDA-MB-231 and MCF-7 breast cancer cells demonstrated that these compounds were more potent antiproliferative agents than cisplatin. In our study the induction of apoptosis by Pt10 and Pt11 in human breast cancer cells was confirmed by several biochemical markers, such as: phosphatidylserine externalization, loss of mitochondrial membrane potential ΔΨm, caspase-3, -8, -9 activity, and DNA degradation. Pt10 and Pt11 induce apoptosis of breast cancer cells via mechanisms dependent on caspases activation and associated with mitochondrial membrane potential disruption.
Figure optionsDownload as PowerPoint slideHighlights
► We investigates the influence of novel dinuclear platinum(II) compounds on growth and viability of MDA-MB-231 and MCF-7 breast cancer cells.
► We studied the induction of apoptosis by these compounds in human breast cancer cells.
► The results demonstrate that dinuclear platinum(II) compounds cause mitochondrial dysfunction and the activation of caspases’ cascade.
Journal: Environmental Toxicology and Pharmacology - Volume 35, Issue 2, March 2013, Pages 254–264