Key Points
- To determine the antitumor-promoting mechanisms and efficacy of (−)-epigallocatechin gallate (EGCG), the primary polyphenol in green tea, in skin carcinogenesis models.
- Assessed EGCG inhibition of [3H]TPA binding to mouse skin particulate fractions and its effect on teleocidin-induced protein kinase C activation.
- Conducted a 25-week two-stage mouse skin carcinogenesis study using 7,12-dimethylbenz(a)anthracene (DMBA) initiation followed by teleocidin promotion with or without EGCG application.
- EGCG decreased phorbol ester receptor counts in mouse skin particulate fractions and inhibited teleocidin-mediated protein kinase C activation.
- At week 25 of two-stage carcinogenesis, skin tumors occurred in 13% of mice treated with DMBA plus teleocidin and EGCG compared to 53% in mice treated with DMBA plus teleocidin alone.
- The average tumor yield per mouse was 0.1 in the DMBA plus teleocidin and EGCG group compared to 2.1 in the DMBA plus teleocidin group, with zero tumors occurring in DMBA-only or teleocidin-plus-EGCG controls.
Structured PICO
Does EGCG prevent tumor promotion by teleocidin in a mouse skin carcinogenesis model?
PPopulationMouse skin model (two-stage carcinogenesis experiment)
IIntervention(-)-Epigallocatechin gallate (EGCG) added to 7,12-dimethylbenz(a)anthracene (DMBA) plus teleocidin
CComparatorDMBA plus teleocidin alone (and other controls: DMBA alone, teleocidin and EGCG alone)
OOutcomeTumor formation (percentage of mice with tumors and average number of tumors per mouse)surrogate
EGCG, the main polyphenolic constituent of green tea, inhibits tumor promotion by teleocidin in a mouse skin carcinogenesis model.