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Cancer Cell death Cell cycle Cytoskeleton Exo/endocytosis Differentiation Division Organelles Signalling Stem cells Trafficking
Cell Biology International (2005) 29, 884–889 (Printed in Great Britain)
Effect of phenols on natural killer (NK) cell-mediated death in the K562 human leukemic cell line
George V.Z. Dedoussis*, Andriana C. Kaliora and Nikolaos K. Andrikopoulos
Department of Science of Dietetics-Nutrition, Harokopio University, 70 El. Venizelou Street, 17671 Kallithea, Athens, Greece


Abstract

Cancer disease is a major cause of death in Western societies. Epidemiologically, antioxidant phenols have been associated with diminished incidence of cancer, while experimentally, they have cytotoxic effects on cancer cells. The aim of this study was to clarify whether natural antioxidant phenols render K562 human leukemic cells more susceptible to natural killer (NK) cell apoptosis and/or necrosis. K562 cells were pre-incubated with 7 different phenols (p-hydroxy benzoic acid, syringic acid, ferulic acid, p-coumaric acid, o-coumaric acid, gallic acid, and rutin) individually and afterwards targeted with NK cells at a ratio 1/5. Percentages of apoptotic and necrotic cells were assayed via flow cytometric analysis of annexin V and PI-stained cells. For the morphological assessment, cells were stained with acridine orange and ethidium bromide and were examined under a fluorescence microscope. Pre-treatment with gallic acid significantly rendered K562 cells more susceptible to NK cell-mediated necrosis, while pre-treatment with rutin significantly rendered K562 cells more susceptible to apoptosis. Gallic acid and rutin exert anticarcinogenic activity via the enhancement of K562 cell susceptibility to NK cell-mediated necrosis and apoptosis, respectively.


Key words: Phenols, Natural killer cells, K562 cells, Apoptosis, Cancer.

*Corresponding author. Tel.: +30 210 9549304; fax: +30 210 9577050.


Received 8 May 2005/14 June 2005; accepted 13 July 2005

doi:10.1016/j.cellbi.2005.07.006


ISSN Print: 1065-6995
ISSN Electronic: 1095-8355
Published by Portland Press Limited on behalf of the International Federation for Cell Biology (IFCB)