Medulloblastoma cell invasion is inhibited by green tea (−)epigallocatechin-3-gallate

• Published in: Journal of cellular biochemistry Vol. 90; no. 4; pp. 745 - 755
• Main Authors: Pilorget, Anthony, Berthet, Virginie, Luis, José, Moghrabi, Albert, Annabi, Borhane, Béliveau, Richard
• Format: Journal Article
• Language: English
• Published: Hoboken Wiley Subscription Services, Inc., A Wiley Company 01.11.2003
• Subjects: Apoptosis - drug effects; Caspase 3; Caspases - metabolism; Catechin - analogs & derivatives; Catechin - pharmacology; Catechin - therapeutic use; cell adhesion; Cell Adhesion - drug effects; Cell Line, Tumor; Cell Movement - drug effects; Collagen - metabolism; EGCG; Flow Cytometry; green tea; Humans; integrin; Integrin beta1 - genetics; Integrin beta1 - metabolism; medulloblastoma; Medulloblastoma - drug therapy; Medulloblastoma - pathology; migration; Neoplasm Invasiveness - prevention & control; Tea - chemistry; Up-Regulation - drug effects
• ISSN: 0730-2312; 1097-4644
• DOI: 10.1002/jcb.10667

Epigallocatechin‐3‐gallate (EGCG), the major green tea polyphenol, can reach the brain following oral intake and could thus act as an anti‐tumoral agent targeting several key steps of brain cancer cells invasive activity. Because integrin‐mediated extracellular matrix recognition is crucial during the cell adhesion processes involved in carcinogenesis, we have investigated the effects of EGCG on different cellular integrins of the pediatric brain tumor‐derived medulloblastoma cell line DAOY. Using flow cytometry, we report the levels of expression of several cell surface integrins in DAOY. These include high expression of α2, α3, and β1 integrins, as well as αv and β3 integrins. Moreover, we provide evidence that EGCG can antagonize DAOY cell migration specifically on collagen by increasing cell adhesive ability through specific gene and protein upregulation of the β1 integrin subunit. Our results suggest that this naturally occurring green tea polyphenol may thus be used as a nutraceutical therapeutic agent in targeting the invasive character of medulloblastomas. © 2003 Wiley‐Liss, Inc.