Please use this identifier to cite or link to this item: http://localhost:8080/xmlui/handle/123456789/2719
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dc.contributor.authorSuman Kumar, Tripathy-
dc.contributor.authorUmasankar De-
dc.contributor.authorNiranjan, Dehury-
dc.contributor.authorPaltan, Laha-
dc.contributor.authorManas Kumar, Panda-
dc.contributor.authorHyung, Sik Kim-
dc.contributor.authorSrikanta, Patra-
dc.date.accessioned2017-04-25T06:13:46Z-
dc.date.available2017-04-25T06:13:46Z-
dc.date.issued2016-08-16-
dc.identifier.citationDalton Transation,45:15122–15136en_US
dc.identifier.urihttp://hdl.handle.net/123456789/2719-
dc.description.abstractSix mononuclear Ir complexes (1–6) using polypyridyl-pyrazine based ligands (L1 and L2) and {[cp*IrCl- (μ-Cl)]2 and [(ppy)2Ir(μ-Cl)]2} precursors have been synthesised and characterised. Complexes 1–5 have shown potent anticancer activity against various human cancer cell lines (MCF-7, LNCap, Ishikawa, DU145, PC3 and SKOV3) while complex 6 is found to be inactive. Flow cytometry studies have established that cellular accumulation of the complexes lies in the order 2 > 1 > 5 > 4 > 3 > 6 which is in accordance with their observed cytotoxicity. No changes in the expression of the proteins like PARP, caspase 9 and beclin-1, Atg12 discard apoptosis and autophagy, respectively. Overexpression of CHOP, activation of MAPKs (P38, JNK, and ERK) and massive cytoplasmic vacuolisation collectively suggest a paraptotic mode of cell death induced by proteasomal dysfunction as well as endoplasmic reticulum and mitochondrial stress. An intimate relationship between p53, ROS production and extent of cell death has also been established using p53 wild, null and mutant type cancer cellsen_US
dc.language.isoenen_US
dc.publisherRoyal Society of Chemistryen_US
dc.subjectintrinsicen_US
dc.subjectphenotypesen_US
dc.subjectnonplatinumen_US
dc.subjectmorphologyen_US
dc.titleCyclometallated iridium complexes inducing paraptotic cell death like natural products: synthesis, structure and mechanistic aspectsen_US
dc.typeArticleen_US
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