The DOI matches its Crossref record; 7 of the 7 references it cites were found in a registry or an index.
Cancer prevention by tea: animal studies, molecular mechanisms and human relevance
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“The mechanisms behind the anti-cancer effect of EGCG may be related to inhibiting tumour angiogenesis, antioxidant effects and suppressing the inflammatory processes contributing to transformation, hyperproliferation and initiation of carcinogenesis [57,59].”
From Health Benefits and Chemical Composition of Matcha Green Tea: A Review (2020) · cites this paper as [59]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Lipinski, C. A., Lombardo, F., Dominy, B. W., & Feeney, P. J. (2001) · Advanced Drug Delivery Reviews · doi:10.1016/s0169-409x(00)00129-0 · Cited by 18,139
Tea catechins and polyphenols: Health effects, metabolism, and antioxidant functions
Higdon, J. V., & Frei, B. (2003) · Critical Reviews in Food Science and Nutrition · doi:10.1080/10408690390826464 · Cited by 1,854
Chow, H.-H. S., Hakim, I. A., Vining, D. R., Crowell, J. A., Ranger-Moore, J., Chew, W. M., Celaya, C. A., Rodney, S. R., Hara, Y., & Alberts, D. S. (2005) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-04-2549 · Cited by 400
DNA and RNA as New Binding Targets of Green Tea Catechins
Kuzuhara, T., Sei, Y., Yamaguchi, K., Suganuma, M., & Fujiki, H. (2006) · Journal of Biological Chemistry · doi:10.1074/jbc.m601196200 · Cited by 151 · cited 1×
“The physical binding of EGCG to nucleic acids suggests that DNA and RNA can also be binding targets of green tea catechi”
BackgroundCONNEY, A., ZHOU, S., LEE, M., XIE, J., YANG, C., LOU, Y., & LU, Y. (2007) · Toxicology and Applied Pharmacology · doi:10.1016/j.taap.2006.11.001 · Cited by 53
Self-citationCarter, O., Wang, R., Dashwood, W. M., Orner, G. A., Fischer, K. A., Löhr, C. V., Pereira, C. B., Bailey, G. S., Williams, D. E., & Dashwood, R. H. (2007) · Nutrition and Cancer · doi:10.1080/01635580701308182 · Cited by 43
Wang, R., Dashwood, W. M., Löhr, C. V., Fischer, K. A., Pereira, C. B., Louderback, M., Nakagama, H., Bailey, G. S., Williams, D. E., & Dashwood, R. H. (2008) · Carcinogenesis · doi:10.1093/carcin/bgn051 · Cited by 34
Research works printed but not linked: 113
- Yang, C. S. & Wang, Z. Y. Tea and cancer. J. Natl Cancer Inst. 85, 1038–1049 (1993). This is the first comprehensive review of the cancer preventive activities of tea. · DOI
- Bushman, J. L. Green tea and cancer in humans: a review of the literature. Nutr. Cancer 31, 151–159 (1998). · DOI
- Yang, C. S., Maliakal, P. & Meng, X. Inhibition of carcinogenesis by tea. Annu. Rev. Pharmacol. Toxicol. 42, 25–54 (2002). · DOI · Paper page
- Hou, Z., Lambert, J. D., Chin, K. V. & Yang, C. S. Effects of tea polyphenols on signal transduction pathways related to cancer chemoprevention. Mutat. Res. 555, 3–19 (2004). · DOI
- Lambert, J. D., Hong, J., Yang, G. Y., Liao, J. & Yang, C. S. Inhibition of carcinogenesis by polyphenols: evidence from laboratory investigations. Am. J. Clin. Nutr. 81, 284S–291S (2005). · DOI
- Clark, J. & You, M. Chemoprevention of lung cancer by tea. Mol. Nutr. Food Res. 50, 144–151 (2006). · DOI
- Khan, N., Afaq, F., Saleem, M., Ahmad, N. & Mukhtar, H. Targeting multiple signaling pathways by green tea polyphenol (−)-epigallocatechin-3-gallate. Cancer Res. 66, 2500–2505 (2006). · DOI · Paper page
- Wu, A. H. & Yu, M. C. Tea, hormone-related cancers and endogenous hormone levels. Mol. Nutr. Food Res. 50, 160–169 (2006). · DOI
- Yang, C. S. et al. Possible mechanisms of the cancer-preventive activities of green tea. Mol. Nutr. Food Res. 50, 170–175 (2006). · DOI
- Ju, J., Lu, G., Lambert, J. D. & Yang, C. S. Inhibition of carcinogenesis by tea constituents. Semin. Cancer Biol. 17, 395–402 (2007). · DOI
- Balentine, D. A., Wiseman, S. A. & Bouwens, L. C. The chemistry of tea flavonoids. Crit. Rev. Food Sci. Nutr. 37, 693–704 (1997). This is a comprehensive review of the composition of different types of tea and the chemistry of tea constituents. · DOI
- Valcic, S., Burr, J. A., Timmermann, B. N. & Liebler, D. C. Antioxidant chemistry of green tea catechins. New oxidation products of (−)-epigallocatechin gallate and (−)-epigallocatechin from their reactions with peroxyl radicals. Chem. Res. Toxicol. 13, 801–810 (2000). · DOI
- Sang, S. M. et al. Theadibenzotropolone A, a new type pigment from enzymatic oxidation of (−)-epicatechin and (−)-epigallocatechin gallate and characterized from black tea using LC/MS/MS. Tetrahedron Lett. 43, 7129–7133 (2002). · DOI
- Hou, Z. et al. Mechanism of action of (−)-epigallocatechin-3-gallate: auto-oxidation-dependent inactivation of epidermal growth factor receptor and direct effects on growth inhibition in human esophageal cancer KYSE 150 cells. Cancer Res. 65, 8049–8056 (2005). · DOI
- Lee, M. J. et al. Pharmacokinetics of tea catechins after ingestion of green tea and (−)-epigallocatechin-3-gallate by humans: formation of different metabolites and individual variability. Cancer Epidemiol. Biomarkers Prev. 11, 1025–1032 (2002).
- Chow, H. H. et al. Pharmacokinetics and safety of green tea polyphenols after multiple-dose administration of epigallocatechin gallate and polyphenon E in healthy individuals. Clin. Cancer Res. 9, 3312–3319 (2003). This article reports the detailed pharmacokinetics and safety of green tea polyphenols in humans.
- Chen, L., Lee, M. J., Li, H. & Yang, C. S. Absorption, distribution, elimination of tea polyphenols in rats. Drug Metab. Dispos. 25, 1045–1050 (1997).
- Lambert, J. D. et al. Dose-dependent levels of epigallocatechin-3-gallate in human colon cancer cells and mouse plasma and tissues. Drug Metab. Dispos. 34, 8–11 (2006). · DOI
- Yang, C. S., Sang, S., Lambert, J. D. & Lee, M. J. Bioavailability issues in studying the health effects of plant polyphenolic compounds. Mol. Nutr. Food Res. 52 (Suppl. 1), 139–151 (2008).
- Wang, Z. Y. et al. Inhibition of N-nitrosodiethylamine- and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone-induced tumorigenesis in A/J mice by green tea and black tea. Cancer Res. 52, 1943–1947 (1992). This is the first publication demonstrating the inhibition of lung carcinogenesis by green and black tea.
- Xu, Y., Ho, C. T., Amin, S. G., Han, C. & Chung, F. L. Inhibition of tobacco-specific nitrosamine-induced lung tumorigenesis in A/J mice by green tea and its major polyphenol as antioxidants. Cancer Res. 52, 3875–3879 (1992). This is the first demonstration of the inhibition of lung tumorigenesis by EGCG and caffeine.
- Yang, G. Y. et al. Black tea constituents, theaflavins, inhibit 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK)-induced lung tumorigenesis in A/J mice. Carcinogenesis 18, 2361–2365 (1997). · DOI
- Chung, F. L. et al. Inhibition of lung carcinogenesis by black tea in Fischer rats treated with a tobacco-specific carcinogen: caffeine as an important constituent. Cancer Res. 58, 4096–4101 (1998).
- Mimoto, J. et al. (−)-Epigallocatechin gallate can prevent cisplatin-induced lung tumorigenesis in A/J mice. Carcinogenesis 21, 915–919 (2000). · DOI
- Zhang, Z. et al. A germ-line p53 mutation accelerates pulmonary tumorigenesis: p53-independent efficacy of chemopreventive agents green tea or dexamethasone/myo-inositol and chemotherapeutic agents taxol or adriamycin. Cancer Res. 60, 901–907 (2000).
- Liao, J. et al. Inhibition of lung carcinogenesis and effects on angiogenesis and apoptosis in A/J mice by oral administration of green tea. Nutr. Cancer 48, 44–53 (2004). · DOI
- Schuller, H. M., Porter, B., Riechert, A., Walker, K. & Schmoyer, R. Neuroendocrine lung carcinogenesis in hamsters is inhibited by green tea or theophylline while the development of adenocarcinomas is promoted: implications for chemoprevention in smokers. Lung Cancer 45, 11–18 (2004). · DOI
- Lu, G. et al. Inhibition of adenoma progression to adenocarcinoma in a 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone-induced lung tumorigenesis model in A/J mice by tea polyphenols and caffeine. Cancer Res. 66, 11494–11501 (2006). · DOI
- Landau, J. M., Wang, Z. Y., Yang, G. Y., Ding, W. & Yang, C. S. Inhibition of spontaneous formation of lung tumors and rhabdomyosarcomas in A/J mice by black and green tea. Carcinogenesis 19, 501–507 (1998). · DOI
- Sazuka, M., Murakami, S., Isemura, M., Satoh, K. & Nukiwa, T. Inhibitory effects of green tea infusion on in vitro invasion and in vivo metastasis of mouse lung carcinoma cells. Cancer Lett. 98, 27–31 (1995). · DOI
- Lu, G. et al. Synergistic inhibition of lung tumorigenesis by a combination of green tea polyphenols and atorvastatin. Clin. Cancer Res. 14, 4981–4988 (2008). · DOI
- Lu, Y. et al. A gene expression signature that can predict green tea exposure and chemopreventive efficacy of lung cancer in mice. Cancer Res. 66, 1956–1963 (2006). · DOI
- Li, N. et al. Inhibition of 7,12-dimethylbenz[a]anthracene (DMBA)-induced oral carcinogenesis in hamsters by tea and curcumin. Carcinogenesis 23, 1307–1313 (2002). · DOI
- Wang, Z. Y. et al. Inhibition of N-nitrosomethylbenzylamine-induced esophageal tumorigenesis in rats by green and black tea. Carcinogenesis 16, 2143–2148 (1995). · DOI
- Yamane, T. et al. Inhibition of N-methyl-N'-nitro-N-nitrosoguanidine-induced carcinogenesis by (−)-epigallocatechin gallate in the rat glandular stomach. Cancer Res. 55, 2081–2084 (1995).
- Murugan, R. S. et al. Modulatory effects of black tea polyphenols on oxidant–antioxidant profile and expression of proliferation, apoptosis, and angiogenesis-associated proteins in the rat forestomach carcinogenesis model. J. Gastroenterol. 42, 352–361 (2007). · DOI
- Ju, J. et al. Inhibition of intestinal tumorigenesis in ApcMin/+ mice by (−)-epigallocatechin-3-gallate, the major catechin in green tea. Cancer Res. 65, 10623–10631 (2005). · DOI
- Hao, X. et al. Inhibition of intestinal tumorigenesis in ApcMin/+ mice by green tea polyphenols (polyphenon E) and individual catechins. Nutr. Cancer 59, 62–69 (2007). · DOI
- Xiao, H. et al. Green tea polyphenols inhibit colorectal aberrant crypt foci (ACF) formation and prevent oncogenic changes in dysplastic ACF in azoxymethane-treated F344 rats. Carcinogenesis 29, 113–119 (2008). · DOI
- Liao, S., Umekita, Y., Guo, J., Kokontis, J. M. & Hiipakka, R. A. Growth inhibition and regression of human prostate and breast tumors in athymic mice by tea epigallocatechin gallate. Cancer Lett. 96, 239–243 (1995). · DOI
- Gupta, S., Hastak, K., Ahmad, N., Lewin, J. S. & Mukhtar, H. Inhibition of prostate carcinogenesis in TRAMP mice by oral infusion of green tea polyphenols. Proc. Natl Acad. Sci. USA 98, 10350–10355 (2001). This is the first demonstration of the inhibition of prostate carcinogenesis in a mouse model by green tea polyphenols and related mechanisms. · DOI · Paper page
- Adhami, V. M., Siddiqui, I. A., Ahmad, N., Gupta, S. & Mukhtar, H. Oral consumption of green tea polyphenols inhibits insulin-like growth factor-I-induced signaling in an autochthonous mouse model of prostate cancer. Cancer Res. 64, 8715–8722 (2004). · DOI · Paper page
- Gao, Y. T. et al. Reduced risk of esophageal cancer associated with green tea consumption. J. Natl. Cancer Inst. 86, 855–858 (1994). · DOI
- Fujiki, H., Suganuma, M., Imai, K. & Nakachi, K. Green tea: cancer preventive beverage and/or drug. Cancer Lett. 188, 9–13 (2002). · DOI
- Zhang, M., Holman, C. D., Huang, J. P. & Xie, X. Green tea and the prevention of breast cancer: a case-control study in Southeast China. Carcinogenesis 28, 1074–1078 (2007). · DOI
- Sun, C. L. et al. Urinary tea polyphenols in relation to gastric and esophageal cancers: a prospective study of men in Shanghai, China. Carcinogenesis 23, 1497–1503 (2002). · DOI
- Yuan, J. M., Gao, Y. T., Yang, C. S. & Yu, M. C. Urinary biomarkers of tea polyphenols and risk of colorectal cancer in the Shanghai Cohort Study. Int. J. Cancer 120, 1344–1350 (2007). · DOI
- Sasazuki, S., Inoue, M., Miura, T., Iwasaki, M. & Tsugane, S. Plasma tea polyphenols and gastric cancer risk: a case-control study nested in a large population-based prospective study in Japan. Cancer Epidemiol. Biomarkers Prev. 17, 343–351 (2008). · DOI
- Wu, A. H., Yu, M. C., Tseng, C. C., Hankin, J. & Pike, M. C. Green tea and risk of breast cancer in Asian Americans. Int. J. Cancer 106, 574–579 (2003). · DOI
- Wu, A. H., Tseng, C. C., Van Den Berg, D. & Yu, M. C. Tea intake, COMT genotype, and breast cancer in Asian-American women. Cancer Res. 63, 7526–7529 (2003).
- Bonner, M. R. et al. Green tea consumption, genetic susceptibility, PAH-rich smoky coal, and the risk of lung cancer. Mutat. Res. 582, 53–60 (2005). · DOI
- Li, N., Sun, Z., Han, C. & Chen, J. The chemopreventive effects of tea on human oral precancerous mucosa lesions. Proc. Soc. Exp. Biol. Med. 220, 218–224 (1999).
- Ahn, W. S. et al. Protective effects of green tea extracts (polyphenon E and EGCG) on human cervical lesions. Eur. J. Cancer Prev. 12, 383–390 (2003). · DOI
- Bettuzzi, S. et al. Chemoprevention of human prostate cancer by oral administration of green tea catechins in volunteers with high-grade prostate intraepithelial neoplasia: a preliminary report from a one-year proof-of-principle study. Cancer Res. 66, 1234–1240 (2006). This is the first demonstration that green tea polyphenols prevented the progression of high-grade PIN to prostate cancer. · DOI · Paper page
- Shimizu, M. et al. Green tea extracts for the prevention of metachronous colorectal adenomas: a pilot study. Cancer Epidemiol. Biomarkers Prev. 17, 3020–3025 (2008). · DOI · Paper page
- Srividhya, R., Jyothilakshmi, V., Arulmathi, K., Senthilkumaran, V. & Kalaiselvi, P. Attenuation of senescence-induced oxidative exacerbations in aged rat brain by (−)-epigallocatechin-3-gallate. Int. J. Dev. Neurosci. 26, 217–223 (2008). · DOI
- Senthil Kumaran, V., Arulmathi, K., Srividhya, R. & Kalaiselvi, P. Repletion of antioxidant status by EGCG and retardation of oxidative damage induced macromolecular anomalies in aged rats. Exp. Gerontol. 43, 176–183 (2008). · DOI
- Inami, S. et al. Tea catechin consumption reduces circulating oxidized low-density lipoprotein. Int. Heart J. 48, 725–732 (2007). · DOI
- Hsu, S. P. et al. Chronic green tea extract supplementation reduces hemodialysis-enhanced production of hydrogen peroxide and hypochlorous acid, atherosclerotic factors, and proinflammatory cytokines. Am. J. Clin. Nutr. 86, 1539–1547 (2007). · DOI
- Hakim, I. A. et al. Effect of increased tea consumption on oxidative DNA damage among smokers: a randomized controlled study. J. Nutr. 133, 3303S–3309S (2003). · DOI
- Schwartz, J. L., Baker, V., Larios, E. & Chung, F. L. Molecular and cellular effects of green tea on oral cells of smokers: a pilot study. Mol. Nutr. Food Res. 49, 43–51 (2005). · DOI
- Yang, G. Y., Liao, J., Kim, K., Yurkow, E. J. & Yang, C. S. Inhibition of growth and induction of apoptosis in human cancer cell lines by tea polyphenols. Carcinogenesis 19, 611–616 (1998). · DOI · Paper page
- Na, H. K. & Surh, Y. J. Modulation of Nrf2-mediated antioxidant and detoxifying enzyme induction by the green tea polyphenol EGCG. Food Chem. Toxicol. 46, 1271–1278 (2008). · DOI · Paper page
- Shen, G. et al. Comparison of (−)-epigallocatechin-3-gallate elicited liver and small intestine gene expression profiles between C57BL/56J mice and C57BL/6J/Nrf2 (-/-) mice. Pharm. Res. 22, 1805–1820 (2005). · DOI
- Chow, H. H. et al. Modulation of human glutathione S-transferases by polyphenon E intervention. Cancer Epidemiol. Biomarkers Prev. 16, 1662–1666 (2007). · DOI
- Tang, L. et al. Modulation of aflatoxin biomarkers in human blood and urine by green tea polyphenols intervention. Carcinogenesis 29, 411–417 (2008). · DOI
- Bonkovsky, H. L. Hepatotoxicity associated with supplements containing Chinese green tea (Camellia sinensis). Ann. Intern. Med. 144, 68–71 (2006). · DOI · Paper page
- Lambert, J. D., Sang, S. & Yang, C. S. Possible controversy over dietary polyphenols: benefits vs risks. Chem. Res. Toxicol. 20, 583–585 (2007). This article discusses possible benefits and risks of taking green tea extract as a dietary supplement. · DOI · Paper page
- Tachibana, H., Koga, K., Fujimura, Y. & Yamada, K. A receptor for green tea polyphenol EGCG. Nature Struct. Mol. Biol. 11, 380–381 (2004). This is the first report of the identification of EGCG targets in a cell line. · DOI
- Umeda, D., Yano, S., Yamada, K. & Tachibana, H. Green tea polyphenol epigallocatechin-3-gallate signaling pathway through 67-kDa laminin receptor. J. Biol. Chem. 283, 3050–3058 (2008). · DOI
- Leone, M. et al. Cancer prevention by tea polyphenols is linked to their direct inhibition of antiapoptotic Bcl-2-family proteins. Cancer Res. 63, 8118–8121 (2003).
- Ermakova, S. et al. The intermediate filament protein vimentin is a new target for epigallocatechin gallate. J. Biol. Chem. 280, 16882–16890 (2005). This is the first report of the identification of an EGCG target protein by affinity chromatography and molecular studies. · DOI
- Li, M. et al. Direct inhibition of insulin-like growth factor-I receptor kinase activity by (−)-epigallocatechin-3-gallate regulates cell transformation. Cancer Epidemiol. Biomarkers Prev. 16, 598–605 (2007). · DOI
- He, Z. et al. Fyn is a novel target of (−)-epigallocatechin gallate in the inhibition of JB6 C141 cell transformation. Mol. Carcinog. 47, 172–183 (2008). · DOI
- Ermakova, S. P. et al. (−)-Epigallocatechin gallate overcomes resistance to etoposide-induced cell death by targeting the molecular chaperone glucose-regulated protein 78. Cancer Res. 66, 9260–9269 (2006). · DOI
- Shim, J. H. et al. (−)-Epigallocatechin gallate regulates CD3-mediated T cell receptor signaling in leukemia through the inhibition of ZAP-70 kinase. J. Biol. Chem. 283, 28370–28379 (2008). · DOI
- Mitsiades, C. S. et al. Inhibition of the insulin-like growth factor receptor-1 tyrosine kinase activity as a therapeutic strategy for multiple myeloma, other hematologic malignancies, and solid tumors. Cancer Cell 5, 221–230 (2004). · DOI · Paper page
- Shimizu, M., Deguchi, A., Hara, Y., Moriwaki, H. & Weinstein, I. B. EGCG inhibits activation of the insulin-like growth factor-1 receptor in human colon cancer cells. Biochem. Biophys. Res. Commun. 334, 947–953 (2005). · DOI
- Vittal, R. et al. Gene expression changes induced by green tea polyphenol (−)-epigallocatechin-3-gallate in human bronchial epithelial 21BES cells analyzed by DNA microarray. Mol. Cancer Ther. 3, 1091–1099 (2004). · DOI
- Dong, Z., Ma, W., Huang, C. & Yang, C. S. Inhibition of tumor promoter-induced activator protein 1 activation and cell transformation by tea polyphenols, (−)-epigallocatechin gallate, and theaflavins. Cancer Res. 57, 4414–4419 (1997).
- Chung, J. Y., Huang, C., Meng, X., Dong, Z. & Yang, C. S. Inhibition of activator protein 1 activity and cell growth by purified green tea and black tea polyphenols in H-ras-transformed cells: structure–activity relationship and mechanisms involved. Cancer Res. 59, 4610–4617 (1999).
- Chung, J. Y., Park, J. O., Phyu, H., Dong, Z. & Yang, C. S. Mechanisms of inhibition of the Ras–MAP kinase signaling pathway in 30.7b Ras 12 cells by tea polyphenols (−)-epigallocatechin-3-gallate and theaflavin-3,3′-digallate. FASEB J. 15, 2022–2024 (2001). · DOI
- Liang, Y. C., Lin-Shiau, S. Y., Chen, C. F. & Lin, J. K. Inhibition of cyclin-dependent kinases 2 and 4 activities as well as induction of Cdk inhibitors p21 and p27 during growth arrest of human breast carcinoma cells by (−)-epigallocatechin-3-gallate. J. Cell Biochem. 75, 1–12 (1999). · DOI
- Nam, S., Smith, D. M. & Dou, Q. P. Ester bond-containing tea polyphenols potently inhibit proteasome activity in vitro and in vivo. J. Biol. Chem. 276, 13322–13330 (2001). · DOI
- Gupta, S., Ahmad, N., Nieminen, A. L. & Mukhtar, H. Growth inhibition, cell-cycle dysregulation, and induction of apoptosis by green tea constituent (−)-epigallocatechin-3-gallate in androgen-sensitive and androgen-insensitive human prostate carcinoma cells. Toxicol. Appl. Pharmacol. 164, 82–90 (2000). · DOI
- Gupta, S., Hussain, T. & Mukhtar, H. Molecular pathway for (−)-epigallocatechin-3-gallate-induced cell cycle arrest and apoptosis of human prostate carcinoma cells. Arch. Biochem. Biophys. 410, 177–185 (2003). · DOI · Paper page
- Smith, D. M. et al. Synthetic analogs of green tea polyphenols as proteasome inhibitors. Mol. Med. 8, 382–392 (2002). · DOI
- Garbisa, S. et al. Tumor invasion: molecular shears blunted by green tea. Nature Med. 5, 1216 (1999). · DOI
- Garbisa, S. et al. Tumor gelatinases and invasion inhibited by the green tea flavanol epigallocatechin-3-gallate. Cancer 91, 822–832 (2001). · DOI
- Annabi, B. et al. Green tea polyphenol (−)-epigallocatechin 3-gallate inhibits MMP-2 secretion and MT1-MMP-driven migration in glioblastoma cells. Biochim. Biophys. Acta 1542, 209–220 (2002). · DOI
- Taniguchi, S. et al. Effect of (−)-epigallocatechin gallate, the main constituent of green tea, on lung metastasis with mouse B16 melanoma cell lines. Cancer Lett. 65, 51–54 (1992). · DOI
- Fang, M. Z. et al. Tea polyphenol (−)-epigallocatechin-3-gallate inhibits DNA methyltransferase and reactivates methylation-silenced genes in cancer cell lines. Cancer Res. 63, 7563–7570 (2003).
- Navarro-Peran, E. et al. The antifolate activity of tea catechins. Cancer Res. 65, 2059–2064 (2005). · DOI
- Shin, E. S. et al. Catechin gallates are NADP+-competitive inhibitors of glucose-6-phosphate dehydrogenase and other enzymes that employ NADP+ as a coenzyme. Bioorg. Med. Chem. 16, 3580–3586 (2008). · DOI
- Ishii, T. et al. Covalent modification of proteins by green tea polyphenol (−)-epigallocatechin-3-gallate through autoxidation. Free Radic. Biol. Med. 45, 1384–1394 (2008). · DOI
- Lo, H. W. & Hung, M. C. Nuclear EGFR signalling network in cancers: linking EGFR pathway to cell cycle progression, nitric oxide pathway and patient survival. Br. J. Cancer 94, 184–188 (2006). · DOI
- Liang, Y. C., Lin-shiau, S. Y., Chen, C. F. & Lin, J. K. Suppression of extracellular signals and cell proliferation through EGF receptor binding by (−)-epigallocatechin gallate in human A431 epidermoid carcinoma cells. J. Cell Biochem. 67, 55–65 (1997). · DOI
- Shimizu, M. et al. (−)-Epigallocatechin gallate and polyphenon E inhibit growth and activation of the epidermal growth factor receptor and human epidermal growth factor receptor-2 signaling pathways in human colon cancer cells. Clin. Cancer Res. 11, 2735–2746 (2005). · DOI · Paper page
- Adachi, S. et al. The inhibitory effect of (−)-epigallocatechin gallate on activation of the epidermal growth factor receptor is associated with altered lipid order in HT29 colon cancer cells. Cancer Res. 67, 6493–6501 (2007). · DOI
- Adachi, S. et al. (−)-Epigallocatechin gallate causes internalization of the epidermal growth factor receptor in human colon cancer cells. Carcinogenesis 29, 1986–1993 (2008). · DOI
- Masuda, M. et al. Epigallocatechin-3-gallate decreases VEGF production in head and neck and breast carcinoma cells by inhibiting EGFR-related pathways of signal transduction. J. Exp. Ther. Oncol. 2, 350–359 (2002). · DOI
- Peschard, P. & Park, M. From Tpr-Met to Met, tumorigenesis and tubes. Oncogene 26, 1276–1285 (2007). · DOI
- Birchmeier, C., Birchmeier, W., Gherardi, E. & Vande Woude, G. F. Met, metastasis, motility and more. Nature Rev. Mol. Cell Biol. 4, 915–925 (2003). · DOI
- Bigelow, R. L. & Cardelli, J. A. The green tea catechins, (−)-Epigallocatechin-3-gallate (EGCG) and (−)-Epicatechin-3-gallate (ECG), inhibit HGF/Met signaling in immortalized and tumorigenic breast epithelial cells. Oncogene 25, 1922–1930 (2006). · DOI
- Lim, Y. C. et al. (−)-Epigallocatechin-3-gallate (EGCG) inhibits HGF-induced invasion and metastasis in hypopharyngeal carcinoma cells. Cancer Lett. 271, 140–152 (2008). · DOI
- Sartippour, M. R. et al. Green tea inhibits vascular endothelial growth factor (VEGF) induction in human breast cancer cells. J. Nutr. 132, 2307–2311 (2002). · DOI
- Rodriguez, S. K. et al. Green tea catechin, epigallocatechin-3-gallate, inhibits vascular endothelial growth factor angiogenic signaling by disrupting the formation of a receptor complex. Int. J. Cancer 118, 1635–1644 (2006). · DOI
- Zhu, B. H. et al. (−)-Epigallocatechin-3-gallate inhibits growth of gastric cancer by reducing VEGF production and angiogenesis. World J. Gastroenterol. 13, 1162–1169 (2007). · DOI
- Sukhthankar, M. et al. A green tea component suppresses posttranslational expression of basic fibroblast growth factor in colorectal cancer. Gastroenterology 134, 1972–1980 (2008). · DOI
- Ciardiello, F. et al. Inhibition of growth factor production and angiogenesis in human cancer cells by ZD1839 (Iressa), a selective epidermal growth factor receptor tyrosine kinase inhibitor. Clin. Cancer Res. 7, 1459–1465 (2001).
- Weinstein, I. B. & Joe, A. Oncogene addiction. Cancer Res. 68, 3077–3080; discussion 3080 (2008). · DOI · Paper page
- Stoner, G. D. et al. Cancer prevention with freeze-dried berries and berry components. Semin. Cancer Biol. 17, 403–410 (2007). · DOI
- Shumway, B. S. et al. Effects of a topically applied bioadhesive berry gel on loss of heterozygosity indices in premalignant oral lesions. Clin. Cancer Res. 14, 2421–2430 (2008). · DOI
Cited by
Schwabe, R. F., & Jobin, C. (2013) · Nature Reviews Cancer · doi:10.1038/nrc3610 · Cited by 1,689
Tea Polyphenols in Promotion of Human Health
Khan, N., & Mukhtar, H. (2018) · Nutrients · doi:10.3390/nu11010039 · Cited by 784
Metabolic fate of polyphenols in the human superorganism
van Duynhoven, J., Vaughan, E. E., Jacobs, D. M., A. Kemperman, R., van Velzen, E. J. J., Gross, G., Roger, L. C., Possemiers, S., Smilde, A. K., Doré, J., et al. (2011) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1000098107 · Cited by 540
The chemistry and biotransformation of tea constituents
Sang, S., Lambert, J. D., Ho, C.-T., & Yang, C. S. (2011) · Pharmacological Research · doi:10.1016/j.phrs.2011.02.007 · Cited by 492
Self-citationThe multifaceted role of reactive oxygen species in tumorigenesis
Kirtonia, A., Sethi, G., & Garg, M. (2020) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-020-03536-5 · Cited by 452
Metadata
- Authors
- Yang, C. S., Wang, X., Lu, G., & Picinich, S. C.
- Venue
- Nature Reviews Cancer
- Published
- 2009-05-14
- Volume
- 9
- Issue
- 6
- Pages
- 429-439
- ISSN
- 1474-175X
- 1474-1768
- Cited by
- 995
- References
- 7
- Language
- en
- Licence
- www.springer.com/tdm (tdm)
- www.springer.com/tdm (vor)
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
Data sources
Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.