Cancer and metastasis: Prevention and treatment by green tea

Department of Dermatology, University of Wisconsin, 4385, Medical Sciences Center, 1300 University Avenue, Madison, WI 53706, USA.
CANCER AND METASTASIS REVIEW (Impact Factor: 7.23). 09/2010; 29(3):435-45. DOI: 10.1007/s10555-010-9236-1
Source: PubMed


Metastasis is the most deadly aspect of cancer and results from several interconnected processes including cell proliferation, angiogenesis, cell adhesion, migration, and invasion into the surrounding tissue. The appearance of metastases in organs distant from the primary tumor is the most destructive feature of cancer. Metastasis remains the principal cause of the deaths of cancer patients despite decades of research aimed at restricting tumor growth. Therefore, inhibition of metastasis is one of the most important issues in cancer research. Several in vitro, in vivo, and epidemiological studies have reported that the consumption of green tea may decrease cancer risk. (-)-Epigallocatechin-3-gallate, major component of green tea, has been shown to inhibit tumor invasion and angiogenesis which are essential for tumor growth and metastasis. This article summarizes the effect of green tea and its major polyphenolic compounds on cancer and metastasis against most commonly diagnosed cancer sites.

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    • "Metastasis is a multi-step process involving complex interactions between the disseminating cancer cells, and their microenvironment (Alizadeh et al., 2014). Cancer metastasis is the cause of 90% of all deaths from cancer and exhibits an outstandingly different situation of clinical characteristics (Khan and Mukhtar, 2010), therefore, agents that inhibit metastasis provide a major advantage in treating cancers. "
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    ABSTRACT: Curcumin has been shown to inhibit migration and invasion of cancer angiogenesis via interacting with key regulatory molecules like NF-kB. Rapidly metabolized and conjugated in the liver, curcumin has the limited systemic bioavailability. Previous results have shown a new light of potential biocompatibility, biodegradability, as well as anti-cancer effects of dendrosomal curcumin (DNC) in biological systems. The present study aims to deliberate the protective effects of DNC on metastatic breast tumor in vitro and in vivo. After the dosing procedure, twenty-seven female mice were divided into 40 and 80mg/kg groups of DNC, along with a control group to investigate the anti-metastatic effects of DNC on mammary tumor-bearing mice. In vitro results showed that the different concentrations of DNC reduced the migration and the adhesion of 4T1 cells after 24h (P<0.05). Under the dosing procedure, DNC was safe at 80mg/kg and lower doses. The treated DNC animals had a higher survival rate and lower metastatic signs (14%) compared to control (100%) (P<0.05). The metastatic tumors were more common in control mice than the treated groups in the lung, the liver and the sternum tissues. Animals treated with DNC had smaller tumor volume in comparison with control group (P<0.05). Final mean tumor volume reached to approximately 1.11, 0.31 and 0.27cm(3) in the control, and 40 and 80mg/kg DNC groups, respectively (P<0.05). Furthermore, suppression of NF-κB expression by DNC led to down-regulation of VEGF, COX-2, and MMP-9 expressions in the breast tumor, the lung, the brain, the spleen and the liver tissues (P<0.05). These outcomes indicate that dendrosomal curcumin has a chemoprotective effect on the breast cancer metastasis through suppression of NF-κB and its regulated gene products. Copyright © 2015 Elsevier B.V. All rights reserved.
    European journal of pharmacology 04/2015; 758. DOI:10.1016/j.ejphar.2015.03.076 · 2.53 Impact Factor
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    • "Cancer disease is a leading cause of death and accounted for 7.6 million deaths in 2008 and could rise to 13.1 million deaths by year 2030 (WHO, 2008). The reason behind such high mortality from cancer is due to their extremely invasive behaviour which typically results in metastasis (Khan and Mukhtar, 2010). Metastasis is an extremely complex process that remains to be a major problem in the management of cancer (Hunter et al., 2008). "
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    ABSTRACT: Kisspeptins (KPs) encoded by the KiSS-1 gene are C-terminally amidated peptide products, including KP- 10, KP-13, KP-14 and KP-54, which are endogenous agonists for the G-protein coupled receptor-54 (GPR54). Functional analyses have demonstrated fundamental roles of KiSS-1 in whole body homeostasis including sexual differentiation of brain, action on sex steroids and metabolic regulation of fertility essential for human puberty and maintenance of adult reproduction. In addition, intensive recent investigations have provided substantial evidence suggesting roles of Kisspeptin signalling via its receptor GPR54 in the suppression of metastasis with a variety of cancers. The present review highlights the latest studies regarding the role of Kisspeptins and the KiSS-1 gene in tumor progression and also suggests targeting the KiSS-1/GPR54 system may represent a novel therapeutic approach for cancers. Further investigations are essential to elucidate the complex pathways regulated by the Kisspeptins and how these pathways might be involved in the suppression of metastasis across a range of cancers.
    Asian Pacific journal of cancer prevention: APJCP 11/2013; 14(11):6215-20. DOI:10.7314/APJCP.2013.14.11.6215 · 2.51 Impact Factor
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    • "EGCG inhibits invasion and metastasis of tumor cells by regulating the activity of enzymes such as MMPs [25– 27, 39]. EGCG inhibits migration, invasion, and spreading of melanoma cells dose dependently [39]. Furthermore, EGCG inhibits tyrosine phosphorylation of focal adhesion kinase and MMP-9 activity [40] [41]. "
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    ABSTRACT: The aim of this study was to investigate the effect of the combination of vorinostat and epigallocatechin-3-gallate against HuCC-T1 human cholangiocarcinoma cells. A novel chemotherapy strategy is required as cholangiocarcinomas rarely respond to conventional chemotherapeutic agents. Both vorinostat and EGCG induce apoptosis and suppress invasion, migration, and angiogenesis of tumor cells. The combination of vorinostat and EGCG showed synergistic growth inhibitory effects and induced apoptosis in tumor cells. The Bax/Bcl-2 expression ratio and caspase-3 and -7 activity increased, but poly (ADP-ribose) polymerase expression decreased when compared to treatment with each agent alone. Furthermore, invasion, matrix metalloproteinase (MMP) expression, and migration of tumor cells decreased following treatment with the vorinostat and EGCG combination compared to those of vorinostat or EGCG alone. Tube length and junction number of human umbilical vein endothelial cells (HUVECs) decreased as well as vascular endothelial growth factor expression following vorinostat and EGCG combined treatment. These results indicate that the combination of vorinostat and EGCG had a synergistic effect on inhibiting tumor cell angiogenesis potential. We suggest that the combination of vorinostat and EGCG is a novel option for cholangiocarcinoma chemotherapy.
    Evidence-based Complementary and Alternative Medicine 06/2013; 2013(3):185158. DOI:10.1155/2013/185158 · 1.88 Impact Factor
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