Green tea and cancer prevention.
ABSTRACT Extracts of green tea and green tea polyphenols have exhibited inhibitory effects against the formation and development of tumors at different organ sites in animals. These include animal models for skin, lung, oral cavity, esophagus, stomach, intestine, colon, liver, pancreas, bladder, mammary gland, and prostate cancers. In addition to suppressing cell proliferation, promoting apoptosis, and modulating signaling transduction, green tea polyphenols, especially (-)-epigallocatechin-3-gallate, also inhibit cell invasion, angiogenesis, and metastasis. This article reviews data on the cancer preventive activities of green tea polyphenols, possible mechanisms involved, and the relationship between green tea consumption and human cancer risk.
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ABSTRACT: Abstract The use of phytochemicals either singly or in combination with other anticancer drugs comes with an advantage of less toxicity and minimal side effects. Signaling Pathways play central role in cell cycle, cell growth, metabolism, etc. Thus, the identification of phytochemicals with promising antagonistic effect on the receptor/s playing key role in single transduction may have better therapeutic application. With this background, phytochemicals were screened against Protease activated receptor 2 (PAR2). PAR2 belong to the superfamily of GPCRs and is an important target for breast cancer. Using in silico methods, this study was able to identify the phytochemicals with promising binding affinity suggesting their therapeutic potential in the treatment of breast cancer. The finding of this study acquires importance as the information on the possible agonist and antagonist of PAR2 is limited due its unique mechanism of activation.Journal of biomolecular Structure & Dynamics 11/2014; DOI:10.1080/07391102.2014.986197 · 2.98 Impact Factor
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ABSTRACT: The cancer stem cell (CSC) model postulates the existence of a small proportion of cancer cells capable of sustaining tumor formation, self-renewal and differentiation. Signal Transducer and Activator of Transcription 3 (STAT3) signaling is known to be selectively activated in breast CSC populations. However, it is yet to be determined which molecular mechanisms regulate STAT3 signaling in CSCs and what chemopreventive agents are effective for suppressing CSC growth. The aim of this study was to examine the potential efficacy of curcumin and epigallocatechin gallate (EGCG) against CSC and to uncover the molecular mechanisms of their anticancer effects. To suppress the CSC phenotype, two breast cancer cell lines (MDA-MB-231 cells and MCF7 cells transfected with HER2) were treated with curcumin (10 μM) with or without EGCG (10 μM) for 48 h. We used tumor-sphere formation and wound-healing assays to determine CSC phenotype. To quantify CSC populations, Fluorescence-activated cell sorting profiling was monitored. STAT3 phosphorylation and interaction with Nuclear Factor-kB (NFkB) were analyzed by performing western blot and immunoprecipitation assays. Combined curcumin and EGCG treatment reduced the cancer stem-like Cluster of differentiation 44 (CD44)-positive cell population. Western blot and immunoprecipitation analyses revealed that curcumin and EGCG specifically inhibited STAT3 phosphorylation and STAT3-NFkB interaction was retained. This study suggests that curcumin and EGCG function as antitumor agents for suppressing breast CSCs. STAT3 and NFκB signaling pathways could serve as targets for reducing CSCs leading to novel targeted-therapy for treating breast cancer. Copyright© 2015 International Institute of Anticancer Research (Dr. John G. Delinassios), All rights reserved.Anticancer research 01/2015; 35(1):39-46. · 1.87 Impact Factor
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ABSTRACT: This study is to compare the effects of green tea polyphenol (GTP) pre-treatment with those of GTP post-treatment on cisplatin (CP)-induced nephrotoxicity in rat. Male Sprague-Dawley rats were randomly divided into six groups. Animals in the control group received 0.9% saline (intraperitoneal); animals in the GTP group received 0.9% saline and GTP (0.2% GTP as their sole source of drinking water); the CP group received only CP (7 mg/kg, intraperitoneal); the CP+preGTP group received GTP from two days before CP to four days after CP and the CP+postGTP group received GTP for four days after CP. CP-induced renal toxicity was evaluated by plasma creatinine and blood urea nitrogen (BUN) concentrations; kidney tissue γ-glutamyl transpeptidase (GGT) and alkaline phosphatase (AP) activities and histopathological examinations. High serume creatinine and BUN concentrations were observed in CP treated rats. The GGT and AP activites were lower in kidney of CP treated rats compared to control rats. In addition, treatment with CP resulted in development of a marked tubular necrosis, and tubular dilation in kidney of rats. Pretreatment with GTP resulted in markedly reduced elevation of serum creatinine and BUN amounts and changes of GGT and AP activity in kidney induced by CP. CP-induced histopathological changes, including tubular necrosis and dilation, were ameliorated in GTP pre-treated rats, compared to CP alone or GTP post-treated rats. These results demonstrate that GTP might have some protective effect against CP-induced nephrotoxicity in rat, and GTP pre-treatment was more effective than GTP post-treatment on reduction of CP-induced renal dysfunction.11/2014; 57(6):464-470. DOI:10.5468/ogs.2014.57.6.464