Green tea extract, epigallocatechin-3-gallate, inhibits the growth and invasive ability of human glioma cells.
نویسندگان
چکیده
Epigallocatechin-3-gallate (EGCG) is a major constituent of green tea, but its effects on glioma cell growth have not been reported. The aim of this study was to investigate the anticancer effect of EGCG on the growth and invasive ability of glioma cells, as well as the molecular mechanisms responsible for it. Two glioma cell lines were treated with EGCG, and its effect on cell proliferation and invasive ability was studied using the MTT, Matrigel invasion and 3-D collagen colony forming assays. Our results demonstrate that EGCG treatment leads to a decrease in cell viability and the S-phase cell fraction in a dose-dependent manner. In addition, invasive ability was significantly suppressed in the EGCG-treated cells. Furthermore, the anticancer effect of EGCG was associated with increased expression of p27 and E-cadherin. Our results suggest that EGCG is a potential anticancer agent against glioma, and that its effect may be mediated through the upregulation of p27 and E-cadherin.
منابع مشابه
Epigallocatechin-3-Gallate Inhibits Stem-Like Inflammatory Breast Cancer Cells
Inflammatory Breast Cancer (IBC) is a highly aggressive form of cancer characterized by high rates of proliferation, lymphangiogenesis and metastasis, and an overall poor survival. As regular green tea consumption has been associated with improved prognosis of breast cancer patients, including decreased risk of recurrence, here the effects of the green tea polyphenol epigallocatechin-3-gallate ...
متن کاملGreen tea polyphenol epigallocatechin-3 gallate inhibits Her-2/neu signaling, proliferation, and transformed phenotype of breast cancer cells.
Overexpression of the epidermal growth factor receptor family member Her-2/neu in breast cancer is associated with poor prognosis. With evidence accumulating for a chemopreventive role of green tea polyphenols, the effects of epigallocatechin-3 gallate (EGCG) on Her-2/neu-overexpressing breast cancer cells were examined. EGCG inhibited mouse mammary tumor virus (MMTV)-Her-2/neu NF639 cell growt...
متن کاملGreen tea catechins and vitamin E inhibit angiogenesis of human microvascular endothelial cells through suppression of IL-8 production.
Epidemiological and animal studies have indicated that consumption of green tea and high vitamin E intake are associated with a reduced risk of developing certain forms of cancer. However, the inhibitory mechanism of green tea catechins and vitamin E in angiogenesis, an important process in tumor growth, has not been well established. In the present study, alpha-tocopherol and several major cat...
متن کاملGreen Tea Catechins Reduce Invasive Potential of Human Melanoma Cells by Targeting COX-2, PGE2 Receptors and Epithelial-to-Mesenchymal Transition
Melanoma is the most serious type of skin disease and a leading cause of death from skin disease due to its highly metastatic ability. To develop more effective chemopreventive agents for the prevention of melanoma, we have determined the effect of green tea catechins on the invasive potential of human melanoma cells and the molecular mechanisms underlying these effects using A375 (BRAF-mutated...
متن کاملInhibitory effects of green tea polyphenols on growth and cellular adherence of an oral bacterium, Porphyromonas gingivalis.
Effects of polyphenolic compounds isolated from green tea (Camellia sinensis) on the growth and adherence of Porphyromonas gingivalis onto human buccal epithelial cells were investigated. Green tea polyphenols, especially (-)-epigallocatechin gallate (EGCg) which is a dominant component of tea polyphenols, completely inhibited the growth and adherence of P. gingivalis onto the buccal epithelial...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید
ثبت ناماگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید
ورودعنوان ژورنال:
- Molecular medicine reports
دوره 1 5 شماره
صفحات -
تاریخ انتشار 2008