Cancer chemoprevention with green tea catechins by targeting receptor tyrosine kinases
Recent studies indicate that receptor tyrosine kinases (RTKs), which play important roles in cell proliferation, are one of the possible targets of green tea catechins (GTCs) in cancer cell growth inhibition. (−)‐Epigallocatechin‐3‐gallate (EGCG), the major catechin in green tea, inhibits cell proli...
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Veröffentlicht in: | Molecular nutrition & food research 2011-06, Vol.55 (6), p.832-843 |
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description | Recent studies indicate that receptor tyrosine kinases (RTKs), which play important roles in cell proliferation, are one of the possible targets of green tea catechins (GTCs) in cancer cell growth inhibition. (−)‐Epigallocatechin‐3‐gallate (EGCG), the major catechin in green tea, inhibits cell proliferation and induces apoptosis in various types of cancer cells, including colorectal cancer and hepatocellular carcinoma cells, by blocking the activation of the epidermal growth factor receptor (EGFR) family of RTKs. EGCG inhibits the activation of insulin‐like growth factor‐1 receptor (IGF‐1R) and VEGFR2, the other members of the RTK family, and this effect is also associated with the anticancer and chemopreventive properties of this agent. EGCG suppresses the activation of EGFR in part by altering membrane lipid organization and causing the subsequent inhibition of the dimerization and activation of this receptor. Preliminary trials have shown that GTCs successfully prevent the development and progression of precancerous lesions, such as colorectal adenomas, without causing severe adverse effects. The present report reviews evidence indicating that GTCs exert anticancer and chemopreventive effects by inhibiting the activation of specific RTKs, especially EGFR, IGF‐1R, and VEGFR2, and concludes that targeting RTKs and their related signaling pathways by using tea catechins could be a promising strategy for the prevention of human cancers. |
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(−)‐Epigallocatechin‐3‐gallate (EGCG), the major catechin in green tea, inhibits cell proliferation and induces apoptosis in various types of cancer cells, including colorectal cancer and hepatocellular carcinoma cells, by blocking the activation of the epidermal growth factor receptor (EGFR) family of RTKs. EGCG inhibits the activation of insulin‐like growth factor‐1 receptor (IGF‐1R) and VEGFR2, the other members of the RTK family, and this effect is also associated with the anticancer and chemopreventive properties of this agent. EGCG suppresses the activation of EGFR in part by altering membrane lipid organization and causing the subsequent inhibition of the dimerization and activation of this receptor. Preliminary trials have shown that GTCs successfully prevent the development and progression of precancerous lesions, such as colorectal adenomas, without causing severe adverse effects. The present report reviews evidence indicating that GTCs exert anticancer and chemopreventive effects by inhibiting the activation of specific RTKs, especially EGFR, IGF‐1R, and VEGFR2, and concludes that targeting RTKs and their related signaling pathways by using tea catechins could be a promising strategy for the prevention of human cancers.</description><identifier>ISSN: 1613-4125</identifier><identifier>EISSN: 1613-4133</identifier><identifier>DOI: 10.1002/mnfr.201000622</identifier><identifier>PMID: 21538846</identifier><language>eng</language><publisher>Weinheim: WILEY-VCH Verlag</publisher><subject>Animals ; Anticarcinogenic Agents - pharmacology ; Anticarcinogenic Agents - therapeutic use ; Catechin - pharmacology ; Catechin - therapeutic use ; Chemoprevention ; Colorectal cancer ; EGCG ; Hepatocellular carcinoma ; Humans ; Lipid rafts ; Membrane Microdomains - drug effects ; Membrane Microdomains - metabolism ; Molecular Targeted Therapy ; Neoplasms - metabolism ; Neoplasms - prevention & control ; Phytotherapy ; Plant Extracts - chemistry ; Plant Extracts - pharmacology ; Plant Extracts - therapeutic use ; Protein Kinase Inhibitors - pharmacology ; Protein Kinase Inhibitors - therapeutic use ; Receptor Protein-Tyrosine Kinases - antagonists & inhibitors ; Receptor tyrosine kinase ; Signal Transduction - drug effects ; Tea - chemistry</subject><ispartof>Molecular nutrition & food research, 2011-06, Vol.55 (6), p.832-843</ispartof><rights>Copyright © 2011 WILEY‐VCH Verlag GmbH & Co. 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Nutr. Food Res</addtitle><description>Recent studies indicate that receptor tyrosine kinases (RTKs), which play important roles in cell proliferation, are one of the possible targets of green tea catechins (GTCs) in cancer cell growth inhibition. (−)‐Epigallocatechin‐3‐gallate (EGCG), the major catechin in green tea, inhibits cell proliferation and induces apoptosis in various types of cancer cells, including colorectal cancer and hepatocellular carcinoma cells, by blocking the activation of the epidermal growth factor receptor (EGFR) family of RTKs. EGCG inhibits the activation of insulin‐like growth factor‐1 receptor (IGF‐1R) and VEGFR2, the other members of the RTK family, and this effect is also associated with the anticancer and chemopreventive properties of this agent. EGCG suppresses the activation of EGFR in part by altering membrane lipid organization and causing the subsequent inhibition of the dimerization and activation of this receptor. Preliminary trials have shown that GTCs successfully prevent the development and progression of precancerous lesions, such as colorectal adenomas, without causing severe adverse effects. The present report reviews evidence indicating that GTCs exert anticancer and chemopreventive effects by inhibiting the activation of specific RTKs, especially EGFR, IGF‐1R, and VEGFR2, and concludes that targeting RTKs and their related signaling pathways by using tea catechins could be a promising strategy for the prevention of human cancers.</description><subject>Animals</subject><subject>Anticarcinogenic Agents - pharmacology</subject><subject>Anticarcinogenic Agents - therapeutic use</subject><subject>Catechin - pharmacology</subject><subject>Catechin - therapeutic use</subject><subject>Chemoprevention</subject><subject>Colorectal cancer</subject><subject>EGCG</subject><subject>Hepatocellular carcinoma</subject><subject>Humans</subject><subject>Lipid rafts</subject><subject>Membrane Microdomains - drug effects</subject><subject>Membrane Microdomains - metabolism</subject><subject>Molecular Targeted Therapy</subject><subject>Neoplasms - metabolism</subject><subject>Neoplasms - prevention & control</subject><subject>Phytotherapy</subject><subject>Plant Extracts - chemistry</subject><subject>Plant Extracts - pharmacology</subject><subject>Plant Extracts - therapeutic use</subject><subject>Protein Kinase Inhibitors - pharmacology</subject><subject>Protein Kinase Inhibitors - therapeutic use</subject><subject>Receptor Protein-Tyrosine Kinases - antagonists & inhibitors</subject><subject>Receptor tyrosine kinase</subject><subject>Signal Transduction - drug effects</subject><subject>Tea - chemistry</subject><issn>1613-4125</issn><issn>1613-4133</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkElPwzAUhC0EYilcOSLfOKV4SezkCBUtSFCkiu1mOealNTROsV0g_55UhYobpzd6-mY0GoSOKelTQthZ7SrfZ6TTRDC2hfapoDxJKefbG82yPXQQwishnLKU76I9RjOe56nYR48D7Qx4bGZQNwsPH-CibRz-tHGGpx7A4QgaGx3BzKwLuGxx1H4K0bop9mBgERuPY-ubYB3gN-t0gHCIdio9D3D0c3voYXh5P7hKbu5G14Pzm8TwnLHEaAmia1UUhAATjJZM5zloIsBInmmTl5KIrOBMVpLDiy6qAoguhexeJk15D52ucxe-eV9CiKq2wcB8rh00y6BySVhBCik7sr8mTdc0eKjUwtta-1ZRolZTqtWUajNlZzj5iV6WNbxs8N_tOqBYA592Du0_cep2PJz8DU_WXhsifG282r8pIbnM1NN4pC4mT8-DnD6qjH8DBJKQIQ</recordid><startdate>201106</startdate><enddate>201106</enddate><creator>Shimizu, Masahito</creator><creator>Adachi, Seiji</creator><creator>Masuda, Muneyuki</creator><creator>Kozawa, Osamu</creator><creator>Moriwaki, Hisataka</creator><general>WILEY-VCH Verlag</general><general>WILEY‐VCH Verlag</general><scope>BSCLL</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>201106</creationdate><title>Cancer chemoprevention with green tea catechins by targeting receptor tyrosine kinases</title><author>Shimizu, Masahito ; Adachi, Seiji ; Masuda, Muneyuki ; Kozawa, Osamu ; Moriwaki, Hisataka</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3822-ca7e60319900e2621b2a88ea06ec735ac8b70659327f73eda9f9e0ab67932c443</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Animals</topic><topic>Anticarcinogenic Agents - pharmacology</topic><topic>Anticarcinogenic Agents - therapeutic use</topic><topic>Catechin - pharmacology</topic><topic>Catechin - therapeutic use</topic><topic>Chemoprevention</topic><topic>Colorectal cancer</topic><topic>EGCG</topic><topic>Hepatocellular carcinoma</topic><topic>Humans</topic><topic>Lipid rafts</topic><topic>Membrane Microdomains - drug effects</topic><topic>Membrane Microdomains - metabolism</topic><topic>Molecular Targeted Therapy</topic><topic>Neoplasms - metabolism</topic><topic>Neoplasms - prevention & control</topic><topic>Phytotherapy</topic><topic>Plant Extracts - chemistry</topic><topic>Plant Extracts - pharmacology</topic><topic>Plant Extracts - therapeutic use</topic><topic>Protein Kinase Inhibitors - pharmacology</topic><topic>Protein Kinase Inhibitors - therapeutic use</topic><topic>Receptor Protein-Tyrosine Kinases - antagonists & inhibitors</topic><topic>Receptor tyrosine kinase</topic><topic>Signal Transduction - drug effects</topic><topic>Tea - chemistry</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Shimizu, Masahito</creatorcontrib><creatorcontrib>Adachi, Seiji</creatorcontrib><creatorcontrib>Masuda, Muneyuki</creatorcontrib><creatorcontrib>Kozawa, Osamu</creatorcontrib><creatorcontrib>Moriwaki, Hisataka</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Molecular nutrition & food research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Shimizu, Masahito</au><au>Adachi, Seiji</au><au>Masuda, Muneyuki</au><au>Kozawa, Osamu</au><au>Moriwaki, Hisataka</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cancer chemoprevention with green tea catechins by targeting receptor tyrosine kinases</atitle><jtitle>Molecular nutrition & food research</jtitle><addtitle>Mol. Nutr. Food Res</addtitle><date>2011-06</date><risdate>2011</risdate><volume>55</volume><issue>6</issue><spage>832</spage><epage>843</epage><pages>832-843</pages><issn>1613-4125</issn><eissn>1613-4133</eissn><abstract>Recent studies indicate that receptor tyrosine kinases (RTKs), which play important roles in cell proliferation, are one of the possible targets of green tea catechins (GTCs) in cancer cell growth inhibition. (−)‐Epigallocatechin‐3‐gallate (EGCG), the major catechin in green tea, inhibits cell proliferation and induces apoptosis in various types of cancer cells, including colorectal cancer and hepatocellular carcinoma cells, by blocking the activation of the epidermal growth factor receptor (EGFR) family of RTKs. EGCG inhibits the activation of insulin‐like growth factor‐1 receptor (IGF‐1R) and VEGFR2, the other members of the RTK family, and this effect is also associated with the anticancer and chemopreventive properties of this agent. EGCG suppresses the activation of EGFR in part by altering membrane lipid organization and causing the subsequent inhibition of the dimerization and activation of this receptor. Preliminary trials have shown that GTCs successfully prevent the development and progression of precancerous lesions, such as colorectal adenomas, without causing severe adverse effects. The present report reviews evidence indicating that GTCs exert anticancer and chemopreventive effects by inhibiting the activation of specific RTKs, especially EGFR, IGF‐1R, and VEGFR2, and concludes that targeting RTKs and their related signaling pathways by using tea catechins could be a promising strategy for the prevention of human cancers.</abstract><cop>Weinheim</cop><pub>WILEY-VCH Verlag</pub><pmid>21538846</pmid><doi>10.1002/mnfr.201000622</doi><tpages>12</tpages></addata></record> |
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subjects | Animals Anticarcinogenic Agents - pharmacology Anticarcinogenic Agents - therapeutic use Catechin - pharmacology Catechin - therapeutic use Chemoprevention Colorectal cancer EGCG Hepatocellular carcinoma Humans Lipid rafts Membrane Microdomains - drug effects Membrane Microdomains - metabolism Molecular Targeted Therapy Neoplasms - metabolism Neoplasms - prevention & control Phytotherapy Plant Extracts - chemistry Plant Extracts - pharmacology Plant Extracts - therapeutic use Protein Kinase Inhibitors - pharmacology Protein Kinase Inhibitors - therapeutic use Receptor Protein-Tyrosine Kinases - antagonists & inhibitors Receptor tyrosine kinase Signal Transduction - drug effects Tea - chemistry |
title | Cancer chemoprevention with green tea catechins by targeting receptor tyrosine kinases |
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