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• W2765940012 abstract "Piplartine (piperlongumine) is a plant-derived molecule that has been receiving intense interest due to its anticancer characteristics that target the oxidative stress. In the present paper, two novel piplartine-containing ruthenium complexes [Ru(piplartine)(dppf)(bipy)](PF6)2 (1) and [Ru(piplartine)(dppb)(bipy)](PF6)2 (2) were synthesized and investigated for their cellular and molecular responses on cancer cell lines. We found that both complexes are more potent than metal-free piplartine in a panel of cancer cell lines on monolayer cultures, as well in 3D model of cancer multicellular spheroids formed from human colon carcinoma HCT116 cells. Mechanistic studies uncovered that the complexes reduced the cell growth and caused phosphatidylserine externalization, internucleosomal DNA fragmentation, caspase-3 activation and loss of the mitochondrial transmembrane potential on HCT116 cells. Moreover, the pre-treatment with Z-VAD(OMe)-FMK, a pan-caspase inhibitor, reduced the complexes-induced apoptosis, indicating cell death by apoptosis through caspase-dependent and mitochondrial intrinsic pathways. Treatment with the complexes also caused a marked increase in the production of reactive oxygen species (ROS), including hydrogen peroxide, superoxide anion and nitric oxide, and decreased reduced glutathione levels. Application of N-acetyl-cysteine, an antioxidant, reduced the ROS levels and apoptosis induced by the complexes, indicating activation of ROS-mediated apoptosis pathway. RNA transcripts of several genes, including gene related to the cell cycle, apoptosis and oxidative stress, were regulated under treatment. However, the complexes failed to induce DNA intercalation. In conclusion, the complexes are more potent than piplartine against different cancer cell lines and are able to induce caspase-dependent and mitochondrial intrinsic apoptosis on HCT116 cells by ROS-mediated pathway." @default.
• W2765940012 created "2017-11-10" @default.
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• W2765940012 date "2017-11-01" @default.
• W2765940012 modified "2023-10-10" @default.
• W2765940012 title "Novel piplartine-containing ruthenium complexes: synthesis, cell growth inhibition, apoptosis induction and ROS production on HCT116 cells" @default.
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• W2765940012 cites W1600447993 @default.
• W2765940012 cites W1874427597 @default.
• W2765940012 cites W1964940783 @default.
• W2765940012 cites W1972192602 @default.
• W2765940012 cites W1975830639 @default.
• W2765940012 cites W1977680805 @default.
• W2765940012 cites W1979129905 @default.
• W2765940012 cites W1987561576 @default.
• W2765940012 cites W1993805759 @default.
• W2765940012 cites W1998518433 @default.
• W2765940012 cites W1998722626 @default.
• W2765940012 cites W1998727542 @default.
• W2765940012 cites W2005028774 @default.
• W2765940012 cites W2010023860 @default.
• W2765940012 cites W2010055809 @default.
• W2765940012 cites W2016947475 @default.
• W2765940012 cites W2024073095 @default.
• W2765940012 cites W2025663807 @default.
• W2765940012 cites W2026529043 @default.
• W2765940012 cites W2039150265 @default.
• W2765940012 cites W2040914101 @default.
• W2765940012 cites W2043930391 @default.
• W2765940012 cites W2050850862 @default.
• W2765940012 cites W2057810394 @default.
• W2765940012 cites W2075243573 @default.
• W2765940012 cites W2076628443 @default.
• W2765940012 cites W2081687671 @default.
• W2765940012 cites W2082378174 @default.
• W2765940012 cites W2089782169 @default.
• W2765940012 cites W2092158018 @default.
• W2765940012 cites W2094964158 @default.
• W2765940012 cites W2095201384 @default.
• W2765940012 cites W2101705215 @default.
• W2765940012 cites W2107277218 @default.
• W2765940012 cites W2110186742 @default.
• W2765940012 cites W2123787138 @default.
• W2765940012 cites W2140928624 @default.
• W2765940012 cites W2197659189 @default.
• W2765940012 cites W2199871211 @default.
• W2765940012 cites W2263917576 @default.
• W2765940012 cites W2275933811 @default.
• W2765940012 cites W2281321105 @default.
• W2765940012 cites W2286626775 @default.
• W2765940012 cites W2294327678 @default.
• W2765940012 cites W2295820531 @default.
• W2765940012 cites W2329880015 @default.
• W2765940012 cites W2403949460 @default.
• W2765940012 cites W2407790282 @default.
• W2765940012 cites W2437234167 @default.
• W2765940012 cites W2473200929 @default.
• W2765940012 cites W2520346202 @default.
• W2765940012 cites W2520575280 @default.
• W2765940012 cites W2526296695 @default.
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• W2765940012 cites W2593649520 @default.
• W2765940012 cites W2602035017 @default.
• W2765940012 cites W2618936559 @default.
• W2765940012 cites W2734747394 @default.
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• W2765940012 doi "https://doi.org/10.18632/oncotarget.22248" @default.
• W2765940012 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/5732813" @default.
• W2765940012 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/29262647" @default.
• W2765940012 hasPublicationYear "2017" @default.
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