| Article ID | Journal | Published Year | Pages | File Type | 
|---|---|---|---|---|
| 10900513 | Cancer Letters | 2005 | 7 Pages | 
Abstract
												One of the major goals in chemotherapy is to circumvent anti-apoptotic strategies developed by tumor cells. In a previous paper, we showed that pomolic acid (PA) is able to kill the leukemia cell line K562 and its MDR derivative, Lucena 1. Here, we demonstrated that PA-induced apoptosis of HL-60 cells is dependent on the activation of caspases-3 and -9 and dissipation of the mitochondrial transmembrane potential (ÎÏm). Disruption of ÎÏm precedes caspase activation and is not inhibited by zVAD-fmk indicating mitochondria as the main target of PA. Our data pointed to the potential use of PA to overcome apoptosis resistance.
											Keywords
												APAf-1zVAD-fmkΔΨmPTPANTMDR3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromideDiOC6(3)MTTapoptotic protease activating factor-1Pomolic acidPermeability transition poreCSAadenine nucleotide translocatorApoptosisCancer therapyCyclosporinleukemiaMitochondrial transmembrane potentialMitochondria membrane potentialPropidium iodide
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											Authors
												Janaina Fernandes, Ricardo Weinlich, Rachel Oliveira Castilho, Maria Auxiliadora Coelho Kaplan, Gustavo Pessini Amarante-Mendes, Cerli Rocha Gattass, 
											