Induction Of Apoptosis By Benzamide In K562 Cells Was Triggered By Inhibition Of Poly (ADP-ribosyl)ation Of Protein(s) | 4887
ISSN: 2155-952X

Journal of Biotechnology & Biomaterials
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Induction of apoptosis by benzamide in K562 cells was triggered by inhibition of poly (ADP-ribosyl)ation of protein(s)

3rd World Congress on Biotechnology

Utpal Ghosh and Nitai P. Bhattacharyya

ScientificTracks Abstracts: J Biotechnol Biomater

DOI: 10.4172/2155-952X.S1.009

To investigate the mechanism(s) of apoptosis induction at physiological condition of growth by benzamide, an inhibitor of poly (ADP-ribose) polymerase, we have treated leukemic cell line K562 with various doses of benzamide for a particular time point as well as fixed dose for different time of incubation and measured several apoptotic parameters. We observed that benzamide treatment resulted significant increase of nuclear fragmentation, nucleosomal ladder formation, and activation of caspase-2, caspase-8, caspase-9/caspase-6, caspase-3 in K562 cells. Dose dependent release of cytochrome-c into cytoplasm and translocation of apoptosis inducing factor (AIF) into nucleus was also observed in K562 cells treated with benzamide for 24 h. Increase in nuclear fragmentation and caspase-3 activation were higher in PARP-1 knock down K562 cells compared to the parental K562 cells after treatment with benzamide, implicating that induction of apoptosis by benzamide is due to inhibition of PARP-1. Significant increase in NAD+ level, i.e inhibition of PARP, by 5mM benzamide treatment was the earliest event (5 h) followed by the increase in comet tail (6 h), caspase-2 (6 h), caspase-8 (9 h), caspase-3 (24 h) activation and nuclear fragmentation (24 h). Benzamide treatment (4 h) reduced poly(ADP-ribosyl)ation of cellular proteins in a dose-dependent manner. So, induction of apoptosis by benzamide treatment was correlated with its ability to inhibit general poly (ADP-ribosyl)ation of proteins and increase in the cellular NAD+ pool. We proposed that induced apoptosis by benzamide treatment could be initiated through inhibition of the poly(ADP-ribosyl)ation of unknown protein(s) involved in apoptosis.