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scientific correspondence
190,000 compounds were used to selectinhibitors by Biosym LUDI and DOCKINGprograms. In these calculations, the relative position of inhibitor and receptor (uPA)with the minimum potential energy repre- Epidemiological studies suggest that the the cathechins, destroying any beneficial sents the most probable way of binding.
effects1. Several mechanisms of anticancer activity of cathechins have been postulated, but none seems universal for all cancers1–3.
reduced by green, but not black, tea1. Here binds to uPA, blocking His 57 and Ser 195 subsequently demonstrated that one of the loop of uPA (Fig. 1a). Such localization of tumour size or even cause complete remis- sion of cancers in mice4,5. The known uPA uPA to recognize its substrates and inhibit inhibitors are unlikely to be used in anti- activity in the presence of different concen- inhibitors by computer modelling using the active site of uPA as a template. Coordinates cathechin (EGC) and epicathechin-3 gallate of human uPA were kindly provided by trozyme, which releases a chromogen on C. Phillips6; National Cancer Institute, specific cleavage by uPA. EGCG from two different suppliers showed almost identical to inhibit uPA with that of a well-knowninhibitor, amiloride, and a control samplewhere no inhibitors were used (Fig. 1b).
EGCG is a weaker inhibitor than amiloride,but can be consumed in much higher doseswithout any toxicological effects. Amilorideis administered in a maximum dose of 20 mg per day, whereas a single cup of teacontains 150 mg EGCG, and some tealovers consume up to 10 cups a day1.
likely to have a physiological effect andcould reduce incidence of cancer in humansor the size of cancers already formed.
Theoretically, EGCG might inhibit cancerformation in many different ways; however,we postulate that the well-known anti-cancer activity of green tea is driven by inhi- bition of uPA, one of the most frequently overexpressed enzymes in human cancers.
Jerzy Jankun
Steven H. Selman
Rafal Swiercz*
Department of Urology, and *Department of Physiology and Molecular Medicine, Ewa Skrzypczak-Jankun
1. Yang, C. S. et al. J. Natl Cancer Inst. 85, 1038–1049 (1993).
UK (purple diamonds); amiloride (green squares), and control sample (orange circles). Experimental mixtures 2. Stoner, G. D. & Mukhtar, H. J. Cell. Biochem. 22, 169–180 (1995).
(50 mM Tris with 0.01% Tween 80, 0.01% PEG 8000 buffer; pH 8.8) were incubated with 1 Ȗg of uPA and 3. Fujiki, H. et al. Prev. Med. 21, 503–509 (1992).
4. Harvey, S. R. et al. Clin. Exp. Metastasis 6, 431–450 (1988).
decreasing amounts of inhibitor for 15 min. 100 Ȗl of this mixture was incubated in a 96-well microplate with 5. Jankun, J., Keck, R. W., Skrzypczak-Jankun, E. & Swiercz, R.
50 Ȗl (2.5 mM) Spectrozyme (carbobenzyl-L-(ȍ)-Glu(Ȋ-t-BuO)-Gly-Arg-p-nitroanilide.2C H OH from American Cancer Res. 57, 559–563 (1997).
Diagnostica Inc., Greenwich, Connecticut), for 10 min. Absorbance, which is inversely proportional to the uPA 6. Spargon, G. et al. Structure 3, 681–691 (1995).
inhibitory activity7, was measured at 405 nm on a microplate reader. 7. Achbarou, A. et al. Cancer Res. 54, 2372–2377 (1994).
Nature Macmillan Publishers Ltd 1997


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