Essential role of caspases in epigallocatechin-3-gallate-mediated inhibition of nuclear factor kappaB and induction of apoptosis (original) (raw)
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Cancer Letters, 1998
Green tea components exert many biological effects, including antitumor and cancer preventive activities. In the search for anticancer agents for prostate cancer the inhibitory effects of green tea components were tested on the prostate cancer cell lines LNCaP, PC-3 and DU145. (−)-Epigallocatechin-3-gallate (EGCG) proved to be the most potent catechin at inhibiting cell growth. The inhibition induced by EGCG was found to occur via apoptotic cell death as shown by changes in nuclear morphology and DNA fragmentation. Thus, we report the first evidence that EGCG is the active component in green tea and induces apoptosis in human prostate cancer cells.
International journal of oncology, 2013
Growing evidence suggests that the flavonoid epigallocatechin-3-gallate (EGCG), notably abundant in green tea, has health-promoting properties. We examined the effect of EGCG on cell survival and apoptosis in the prostate cancer cell line PC3. Cell survival was reduced and apoptosis increased significantly with a low dose of 1 µM EGCG. The ability of the anticancer drug cisplatin to promote apoptosis was enhanced by EGCG. Furthermore, EGCG, both alone and in combination with cisplatin, promoted the expression of the pro-apoptotic splice isoform of caspase 9.
Preclinical Activities of Epigallocatechin Gallate in Signaling Pathways in Cancer
Molecules
Epigallocatechin gallate (EGCG) is the main bioactive component of catechins predominantly present in various types of tea. EGCG is well known for a wide spectrum of biological activities as an anti-oxidative, anti-inflammatory, and anti-tumor agent. The effect of EGCG on cell death mechanisms via the induction of apoptosis, necrosis, and autophagy has been documented. Moreover, its anti-proliferative action has been demonstrated in many cancer cell lines. It was also involved in the modulation of cyclooxygenase-2, oxidative stress and inflammation of different cellular processes. EGCG has been reported as a promising agent target for plasma membrane proteins, such as epidermal growth factor receptor. In addition, it has been demonstrated a mechanism of action relying on the inhibition of ERK1/2, p38 MAPK, NF-κB, and vascular endothelial growth factor. Furthermore, EGCG and its derivatives were used in proteasome inhibition and they were involved in epigenetic mechanisms. In summary...
Apoptosis, 2011
Animal tumor bioassays and in vitro cell culture systems have demonstrated that epigallocatechin-3-Ogallate (EGCG), the predominant catechin in green tea, possesses anti-proliferative and pro-apoptotic effects on various cancer cells and tumors. In this study, we investigated the effects of EGCG on cell growth, cell cycle progression, and apoptosis in human fibrosarcoma HT-1080 cells. The involvement of p53, Bcl-2, Bax, caspases, and nuclear factor-jB (NF-jB) was examined as a mechanism for the anti-cancer activity of EGCG. Time-dependent intracellular trafficking of EGCG was also determined using fluorescein isothiocyanate (FITC)-conjugated EGCG (FITC-EGCG). Our data show that EGCG treatment caused dose-dependent cell growth inhibition, cell cycle arrest at the G 0 /G 1 phase, and DNA fragmentation suggesting the induction of apoptosis in HT-1080 cells. Immunoblot analysis revealed that the expression of p53, caspase-7 and-9 as well as the ratio of Bax/Bcl-2 protein increased significantly with higher EGCG concentrations and longer incubation times. Moreover, expression of phosphorylated NF-jB/p65 in HT-1080 cells was inhibited by EGCG treatment in a dose-dependent manner, while that of unphosphorylated NF-jB/p65 remained unaffected. Here we also reveal time-dependent internalization of FITC-EGCG into the cytosol of HT-1080 cells and its subsequent nuclear translocation. These results suggest that EGCG may interrupt exogenous signals directed towards genes involved in proliferation and cell cycle progression. Taken together, our data indicate that HT-1080 apoptosis may be mediated through the induction of p53 and caspases by the pro-oxidant activity of internalized EGCG, as well as suppression of Bcl-2 and phosphorylated NF-jB by the antioxidant activity of EGCG.
Targeting Multiple Signaling Pathways by Green Tea Polyphenol ()-Epigallocatechin-3Gallate
Cell signaling pathways, responsible for maintaining a balance between cell proliferation and death, have emerged as rational targets for the management of cancer. Emerging data amassed from various laboratories around the world suggests that green tea, particularly its major polyphenolic constituent (À)-epigallocatechin-3-gallate (EGCG), possesses remarkable cancer chemopreventive and therapeutic potential against various cancer sites in animal tumor bioassay systems and in some human epidemiologic studies. EGCG has been shown to modulate multiple signal transduction pathways in a fashion that controls the unwanted proliferation of cells, thereby imparting strong cancer chemopreventive as well as therapeutic effects. This review discusses the modulations of important signaling events by EGCG and their implications in cancer management. (Cancer Res 2006; 66(5): 2500-5) Requests for reprints: Hasan Mukhtar,
Cancer preventive and therapeutic effects of EGCG, the major polyphenol in green tea
Egyptian Journal of Basic and Applied Sciences, 2018
(-)-epigallocatechin-3-gallate (EGCG), the major bioactive catechin in green tea (GT) has been studied for almost past thirty years as an agent initially for its cancer chemoprevention effects and then for its cancer chemotherapeutic ability. This agent has shown considerable anti-cancer effects in a variety of preclinical cell culture and animal model systems. However, its clinical application to human patients is hampered by a variety of reasons that includes its stability and bioavailability. As a result, an increased number of studies assessing the effects derived from the use of EGCG are been employed in combination with other agents or by utilizing innovative carrier settings. Here, we summarize the current understanding of the anticancer effects of EGCG and its effects with other combinations on different kinds of cancers. Further, we also present the available information for the possible mechanism of action of EGCG.