title: Chemoprevention of oral cancer by green tea.
abstract: Green tea has been a popular beverage for many centuries. Only recently, however, has the anti-cancer power of green tea constituents been unveiled. Green tea polyphenols are found to induce apoptosis (programmed cell death) in many types of tumor cells, including oral cancer cells. However, mechanisms that enable normal cells to evade the apoptotic effect still are not understood. In this study, cell growth and invasion assays combined with apoptosis assays were used to examine the effects of green tea extracts, green tea polyphenols, and the most potent green tea polyphenol, (-)-epigallocatechin-3-gallate (EGCG), on normal human keratinocytes and oral carcinoma cells. The results showed that green tea and its constituents selectively induce apoptosis only in oral carcinoma cells, while EGCG was able to inhibit the growth and invasion of oral carcinoma cells. These differential responses to green tea and its constituents between normal and malignant cells were correlated with the induction of p57, a cell cycle regulator. These data suggest that the chemopreventive effects of green tea polyphenols may involve a p57 mediated survival pathway in normal epithelial cells, while oral carcinoma cells undergo an apoptotic pathway. Therefore, regular consumption of green tea could be beneficial in the prevention of oral cancer.
authors: Department of Oral Biology and Maxillofacial Pathology, School of Dentistry, Medical College of Georgia, Augusta, USA.
authors: Stephen D
authors: SD
authors: Hsu
authors: Baldev B
authors: BB
authors: Singh
authors: Jill B
authors: JB
authors: Lewis
authors: James L
authors: JL
authors: Borke
authors: Douglas P
authors: DP
authors: Dickinson
authors: Laura
authors: L
authors: Drake
authors: Gretchen B
authors: GB
authors: Caughman
authors: George S
authors: GS
authors: Schuster
mesh_terms: D000972:Antineoplastic Agents, Phytogenic / Q000627:therapeutic use*; D017209:Apoptosis / Q000187:drug effects; D002277:Carcinoma / Q000473:pathology / Q000517:prevention & control*; D002392:Catechin / Q000031:analogs & derivatives / Q000627:therapeutic use; D002455:Cell Division / Q000187:drug effects; D002460:Cell Line; D002465:Cell Movement / Q000187:drug effects; D002470:Cell Survival; D018890:Chemoprevention; D050761:Cyclin-Dependent Kinase Inhibitor p57; D004791:Enzyme Inhibitors / Q000378:metabolism; D004847:Epithelial Cells / Q000187:drug effects; D005419:Flavonoids; D006801:Humans; D015603:Keratinocytes / Q000187:drug effects; D009062:Mouth Neoplasms / Q000473:pathology / Q000517:prevention & control*; D009361:Neoplasm Invasiveness / Q000473:pathology / Q000517:prevention & control; D009687:Nuclear Proteins / Q000378:metabolism; D010636:Phenols / Q000627:therapeutic use*; D010936:Plant Extracts / Q000627:therapeutic use; D011108:Polymers / Q000627:therapeutic use*; D013662:Tea; D014407:Tumor Cells, Cultured; D014568:Urokinase-Type Plasminogen Activator / Q000037:antagonists & inhibitors
chemical_list: D000972:Antineoplastic Agents, Phytogenic; C493964:CDKN1C protein, human; D050761:Cyclin-Dependent Kinase Inhibitor p57; D004791:Enzyme Inhibitors; D005419:Flavonoids; D009687:Nuclear Proteins; D010636:Phenols; D010936:Plant Extracts; D011108:Polymers; D013662:Tea; D002392:Catechin; C045651:epigallocatechin gallate; D014568:Urokinase-Type Plasminogen Activator