NDLI: In vitro antiproliferative and apoptosis-inducing properties of a mononuclear copper(II) complex with dppz ligand, in two genotypically different breast cancer cell lines

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In vitro antiproliferative and apoptosis-inducing properties of a mononuclear copper(II) complex with dppz ligand, in two genotypically different breast cancer cell lines

Content Provider	Springer Nature Link
Author	Dhivya, Rajakumar Jaividhya, Paramasivam Riyasdeen, Anvarbatcha Palaniandavar, Mallayan Mathan, Ganeshan Akbarsha, Mohammad Abdulkader
Copyright Year	2015
Abstract	In the background that there is concerted effort to discover newer metal-based cancer chemotherapeutic agents that could overcome the limitations in cisplatin and that copper, a biocompatible and redox-active metal, offers potential as alternative to cisplatin, the present study was undertaken to investigate the in vitro anti-proliferative properties of the mononuclear copper(II)complex [Cu(L)(diimine)] + where LH = 2-[(2-dimethylaminoethylimino)methyl]phenol and diimine = dipyrido[3,2-a:2′,3′-c]phenazine (dppz) using breast cancer cell lines MCF-7 (ER+ve and p53WT) and MDA-MB-231(ER−ve and p53mutant) when cisplatin was used as positive control. The complex affected the viability of both the cell lines in dose—as well as duration-dependent manner as revealed in the MTT assay. The 24 and 48 h IC50 of the complex were several times lesser than those of cisplatin, and within this huge difference the efficacy of the complex was much superior with MCF-7 cell compared to MDA-MB-231 cell. The cell death was preferentially apoptosis, though necrosis also occurred to a certain extent. These inferences were substantiated by AO/EB fluorescent staining, Hoechst staining, assessment of mitochondrial transmembrane potential, comet assay for DNA damage, DCFH assay for reactive oxygen species (ROS) generation and Western blot of apoptosis–related proteins. Thus, the copper(II) dppz complex under investigation is much more efficient than cisplatin in affecting viability of the breast cancer cells. The underlying mechanism appears to be DNA damage-primed (in view of the known intercalation mode of binding of the complex with DNA) and ROS-associated mitochondria-mediated intrinsic apoptosis to a great extent but necrosis also has a role to a certain extent, which may also be a PARP-mediated cell death independent of apoptosis. Within the purview of this conclusion, the results indicate that the ER and/or p53 genotypes have a bearing on the efficacy of the complex as a cytotoxic agent since the response in the ER−ve and p53mutant MDA-MB-231 cell was not so prominent as in ER+ve and p53WT MCF-7 cell. Taken together, the complex has been shown to be a potential DNA damaging agent and, in the light of the superiority of the complex over cisplatin, we are further investigating the possibility of targeted nano-delivery of the complex to the tumor cells. When tested on a normal cell, 3T3, Cu(II)dppz was found to affect its viability but at concentrations very high compared to those for the breast cancer cells. Yet, this is a cause of concern and, therefore, we are working out a strategy for targeted delivery of this complex to the cancer cells only.
Starting Page	929
Ending Page	943
Page Count	15
File Format	PDF
ISSN	09660844
Journal	BioMetals
Volume Number	28
Issue Number	5
e-ISSN	15728773
Language	English
Publisher	Springer Netherlands
Publisher Date	2015-09-03
Publisher Place	Dordrecht
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Copper Apoptosis ROS DNA damage Biochemistry Pharmacology/Toxicology Microbiology Cell Biology Plant Physiology Medicine/Public Health
Content Type	Text
Resource Type	Article
Subject	Metals and Alloys Biochemistry, Genetics and Molecular Biology Biomaterials Agricultural and Biological Sciences

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