Carcinogenesis Advance Access originally published online on February 17, 2005
Carcinogenesis 2005 26(6):1100-1108; doi:10.1093/carcin/bgi048
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Carcinogenesis vol.26 no.6 © Oxford University Press 2005; all rights reserved.
Human epidermal keratinocytes undergo (–)-epigallocatechin-3-gallate-dependent differentiation but not apoptosis
1 Department of Physiology and Biophysics, 2 Department of Dermatology, 3 Department of Biochemistry, 4 Department of Reproductive Biology and 5 Department of Oncology, Case School of Medicine, Cleveland, OH 44106-4970, USA
* To whom correspondence should be addressed at: Department of Physiology/Biophysics, Case Western Reserve University School of Medicine, 2109 Adelbert Road, Cleveland, OH 44106-4970, USA. Tel: +1 216 368 5530; Fax: +1 216 368 5586; Email: rle2{at}po.cwru.edu
Epigallocatechin-3-gallate (EGCG) is an important chemopreventive agent derived from green tea. We recently reported that EGCG treatment enhances keratinocyte differentiation as evidenced by increased human involucrin promoter activity [Balasubramanian,S., Efimova,T. and Eckert,R.L. (2002) J. Biol. Chem., 277, 1828–1836]. In the present paper, we extend these findings and show that EGCG also increases the expression of other differentiation markers—procaspase 14 and type I transglutaminase (TG1). Both TG1 mRNA and protein level, and activity are increased by treatment with EGCG. Increased TG1 activity is evidenced by a direct transglutaminase assay, and by the ability of EGCG to stimulate the covalent incorporation of fluorescein cadaverine substrate into crosslinked intracellular structures. In contrast, type II transglutaminase levels are not altered by EGCG treatment. We also assessed whether EGCG promotes keratinocyte apoptosis. We show that EGCG treatment does not promote the cleavage of procaspase-3, -8, -9 or poly(ADP-ribose) polymerase. Moreover, treatment with the pan-caspase inhibitor, Z-VAD-FMK, does not reverse the EGCG-associated reduction in cell viability. In addition, there is no increase in cells having sub-G1/S DNA content, and no evidence for the release of cytochrome c from the mitochondria. These findings confirm, using several endpoints, that EGCG treatment enhances normal keratinocyte differentiation but does not promote apoptosis.
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