（-）-Epigallocatechin-3-gallate inhibits growth of gastric cancer by reducing VEGF production and angiogenesis
AIM： To investigate the effect of （-）-epigallocatechin-3-gallate （EGCG） on growth of gastric cancer and its possible mechanism. METHODS： Heterotopic tumors were induced by subcutaneously injection of SGC-7901 cells in nude mice. Tumor growth was measured by calipers in two dimensions. Tumor angiogen...
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| Veröffentlicht in: | World journal of gastroenterology : WJG 2007-02, Vol.13 (8), p.1162-1169 |
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| container_title | World journal of gastroenterology : WJG |
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| creator | Zhu, Bao-He Zhan, Wen-Hua Li, Zheng-Rong Wang, Zhao He, Yu-Long Peng, Jun-Sheng Cai, Shi-Rong Ma, Jin-Ping Zhang, Chang-Hua |
| description | AIM： To investigate the effect of （-）-epigallocatechin-3-gallate （EGCG） on growth of gastric cancer and its possible mechanism.
METHODS： Heterotopic tumors were induced by subcutaneously injection of SGC-7901 cells in nude mice. Tumor growth was measured by calipers in two dimensions. Tumor angiogenesis was determined with tumor microvessel density （MVD） by immunohistology. Vascular endothelial growth factor （VEGF） protein level and activation of signal transducer and activator of transcription 3 （Star3） were examined by Western blotting. VEGF mRNA expression was determined by RT-PCR and VEGF release in tumor culture medium by ELISA. VEGF-induced cell proliferation was studied by MTT assay, cell migration by gelatin modified Boyden chamber （Transwell） and in vitro angiogenesis by endothelial tube formation in Matrigel.
RESULTS： Intraperitoneal injection of EGCG inhibited the growth of gastric cancer by 60.4%. MVD in tumor tissues treated with EGCG was markedly reduced. EGCG treatment reduced VEGF protein level in vitro and in vivo. Secretion and mRNA expression of VEGF in tumor cells were also suppressed by EGCG in a dose-dependent manner. This inhibitory effect was associated with reduced activation of Star3, but EGCG treatment did not change the total Star3 expression. EGCG also inhibited VEGF-induced endothelial cell proliferation, migration and tube formation.
CONCLUSION： EGCG inhibits the growth of gastric cancer by reducing VEGF production and angiogenesis, and is a promising candidate for anti-angiogenic treatment of gastric cancer. |
| doi_str_mv | 10.3748/wjg.v13.i8.1162 |
| format | Article |
| fullrecord | <record><control><sourceid>wanfang_jour_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4146988</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><cqvip_id>24306785</cqvip_id><wanfj_id>wjg200708003</wanfj_id><sourcerecordid>wjg200708003</sourcerecordid><originalsourceid>FETCH-LOGICAL-c513t-7ea02037bebc000c2e9ba324eacea08d39017332451f7307b765a56290cc783a3</originalsourceid><addsrcrecordid>eNpVUU1vEzEQtRCIhsKZG7IQ4rbp2LO79l6QUJW2SJW4AFfL63h3HRI7sXcb9R_Af-p_6l-oo0R8HCzreZ7fzLxHyFsGcxSlvNiv-vkdw7mTc8Zq_ozMOGdNwWUJz8mMAYiiQS7OyKuUVgAcseIvyRkTZcVYU87I7vHhV_H48LtYbF2v1-tg9GjN4HyBxQFnRJ0fXOvGRPsY9uNAQ0d7ncboDDXaGxtpe0-jXU7G-Z7-WFxf0W0MGY4ueKr9Mp_ehd56m1x6TV50ep3sm9N9Tr5fLb5d3hS3X6-_XH6-LUzFcCyE1cABRWtbAwCG26bVyEurTa7IJTbABOaHinUCQbSirnRV8waMERI1npNPR93t1G7s0lg_Rr1W2-g2Ot6roJ36v-LdoPpwp0pW1o2UWeDDUWCvfZc3UKswRZ9HVtl1nq0FCYCZ9vHUJ4bdZNOoNi4Zm63zNkxJCSgRZVVl4sWRaGJIKdruzywM1CHNg67KaSon1SHN_OPdvyv85Z_iy4T3J8kh-H6X7VetNj87t7aKlwi1kBU-AT5UqwU</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>70433855</pqid></control><display><type>article</type><title>（-）-Epigallocatechin-3-gallate inhibits growth of gastric cancer by reducing VEGF production and angiogenesis</title><source>MEDLINE</source><source>PubMed Central</source><source>Alma/SFX Local Collection</source><creator>Zhu, Bao-He ; Zhan, Wen-Hua ; Li, Zheng-Rong ; Wang, Zhao ; He, Yu-Long ; Peng, Jun-Sheng ; Cai, Shi-Rong ; Ma, Jin-Ping ; Zhang, Chang-Hua</creator><creatorcontrib>Zhu, Bao-He ; Zhan, Wen-Hua ; Li, Zheng-Rong ; Wang, Zhao ; He, Yu-Long ; Peng, Jun-Sheng ; Cai, Shi-Rong ; Ma, Jin-Ping ; Zhang, Chang-Hua</creatorcontrib><description>AIM： To investigate the effect of （-）-epigallocatechin-3-gallate （EGCG） on growth of gastric cancer and its possible mechanism.
METHODS： Heterotopic tumors were induced by subcutaneously injection of SGC-7901 cells in nude mice. Tumor growth was measured by calipers in two dimensions. Tumor angiogenesis was determined with tumor microvessel density （MVD） by immunohistology. Vascular endothelial growth factor （VEGF） protein level and activation of signal transducer and activator of transcription 3 （Star3） were examined by Western blotting. VEGF mRNA expression was determined by RT-PCR and VEGF release in tumor culture medium by ELISA. VEGF-induced cell proliferation was studied by MTT assay, cell migration by gelatin modified Boyden chamber （Transwell） and in vitro angiogenesis by endothelial tube formation in Matrigel.
RESULTS： Intraperitoneal injection of EGCG inhibited the growth of gastric cancer by 60.4%. MVD in tumor tissues treated with EGCG was markedly reduced. EGCG treatment reduced VEGF protein level in vitro and in vivo. Secretion and mRNA expression of VEGF in tumor cells were also suppressed by EGCG in a dose-dependent manner. This inhibitory effect was associated with reduced activation of Star3, but EGCG treatment did not change the total Star3 expression. EGCG also inhibited VEGF-induced endothelial cell proliferation, migration and tube formation.
CONCLUSION： EGCG inhibits the growth of gastric cancer by reducing VEGF production and angiogenesis, and is a promising candidate for anti-angiogenic treatment of gastric cancer.</description><identifier>ISSN: 1007-9327</identifier><identifier>EISSN: 2219-2840</identifier><identifier>DOI: 10.3748/wjg.v13.i8.1162</identifier><identifier>PMID: 17451194</identifier><language>eng</language><publisher>United States: Department of Gastrointestinal & Pancreatic Surgery, First Affiliated Hospital, Sun Yat-Sen University</publisher><subject>Animals ; Anticarcinogenic Agents - pharmacology ; Anticarcinogenic Agents - therapeutic use ; Carcinoma - drug therapy ; Carcinoma - pathology ; Catechin - analogs & derivatives ; Catechin - pharmacology ; Catechin - therapeutic use ; Cell Line, Tumor ; Cell Movement - drug effects ; Cell Proliferation - drug effects ; Endothelial Cells - drug effects ; Female ; Gastric Cancer ; Gene Expression Regulation, Neoplastic ; Humans ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Neovascularization, Pathologic - drug therapy ; STAT3 Transcription Factor - drug effects ; Stomach Neoplasms - drug therapy ; Stomach Neoplasms - pathology ; Vascular Endothelial Growth Factor A - drug effects ; VEGF生成 ; Xenograft Model Antitumor Assays ; 抑制作用 ; 肿瘤生长 ; 血管发生 ; 表没食子儿茶素-3-没食子酸酯</subject><ispartof>World journal of gastroenterology : WJG, 2007-02, Vol.13 (8), p.1162-1169</ispartof><rights>Copyright © Wanfang Data Co. Ltd. All Rights Reserved.</rights><rights>2007 Baishideng Publishing Group Co., Limited. All rights reserved. 2007</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c513t-7ea02037bebc000c2e9ba324eacea08d39017332451f7307b765a56290cc783a3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Uhttp://image.cqvip.com/vip1000/qk/84123X/84123X.jpg</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4146988/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4146988/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17451194$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhu, Bao-He</creatorcontrib><creatorcontrib>Zhan, Wen-Hua</creatorcontrib><creatorcontrib>Li, Zheng-Rong</creatorcontrib><creatorcontrib>Wang, Zhao</creatorcontrib><creatorcontrib>He, Yu-Long</creatorcontrib><creatorcontrib>Peng, Jun-Sheng</creatorcontrib><creatorcontrib>Cai, Shi-Rong</creatorcontrib><creatorcontrib>Ma, Jin-Ping</creatorcontrib><creatorcontrib>Zhang, Chang-Hua</creatorcontrib><title>（-）-Epigallocatechin-3-gallate inhibits growth of gastric cancer by reducing VEGF production and angiogenesis</title><title>World journal of gastroenterology : WJG</title><addtitle>World Journal of Gastroenterology</addtitle><description>AIM： To investigate the effect of （-）-epigallocatechin-3-gallate （EGCG） on growth of gastric cancer and its possible mechanism.
METHODS： Heterotopic tumors were induced by subcutaneously injection of SGC-7901 cells in nude mice. Tumor growth was measured by calipers in two dimensions. Tumor angiogenesis was determined with tumor microvessel density （MVD） by immunohistology. Vascular endothelial growth factor （VEGF） protein level and activation of signal transducer and activator of transcription 3 （Star3） were examined by Western blotting. VEGF mRNA expression was determined by RT-PCR and VEGF release in tumor culture medium by ELISA. VEGF-induced cell proliferation was studied by MTT assay, cell migration by gelatin modified Boyden chamber （Transwell） and in vitro angiogenesis by endothelial tube formation in Matrigel.
RESULTS： Intraperitoneal injection of EGCG inhibited the growth of gastric cancer by 60.4%. MVD in tumor tissues treated with EGCG was markedly reduced. EGCG treatment reduced VEGF protein level in vitro and in vivo. Secretion and mRNA expression of VEGF in tumor cells were also suppressed by EGCG in a dose-dependent manner. This inhibitory effect was associated with reduced activation of Star3, but EGCG treatment did not change the total Star3 expression. EGCG also inhibited VEGF-induced endothelial cell proliferation, migration and tube formation.
CONCLUSION： EGCG inhibits the growth of gastric cancer by reducing VEGF production and angiogenesis, and is a promising candidate for anti-angiogenic treatment of gastric cancer.</description><subject>Animals</subject><subject>Anticarcinogenic Agents - pharmacology</subject><subject>Anticarcinogenic Agents - therapeutic use</subject><subject>Carcinoma - drug therapy</subject><subject>Carcinoma - pathology</subject><subject>Catechin - analogs & derivatives</subject><subject>Catechin - pharmacology</subject><subject>Catechin - therapeutic use</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement - drug effects</subject><subject>Cell Proliferation - drug effects</subject><subject>Endothelial Cells - drug effects</subject><subject>Female</subject><subject>Gastric Cancer</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Humans</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Nude</subject><subject>Neovascularization, Pathologic - drug therapy</subject><subject>STAT3 Transcription Factor - drug effects</subject><subject>Stomach Neoplasms - drug therapy</subject><subject>Stomach Neoplasms - pathology</subject><subject>Vascular Endothelial Growth Factor A - drug effects</subject><subject>VEGF生成</subject><subject>Xenograft Model Antitumor Assays</subject><subject>抑制作用</subject><subject>肿瘤生长</subject><subject>血管发生</subject><subject>表没食子儿茶素-3-没食子酸酯</subject><issn>1007-9327</issn><issn>2219-2840</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVUU1vEzEQtRCIhsKZG7IQ4rbp2LO79l6QUJW2SJW4AFfL63h3HRI7sXcb9R_Af-p_6l-oo0R8HCzreZ7fzLxHyFsGcxSlvNiv-vkdw7mTc8Zq_ozMOGdNwWUJz8mMAYiiQS7OyKuUVgAcseIvyRkTZcVYU87I7vHhV_H48LtYbF2v1-tg9GjN4HyBxQFnRJ0fXOvGRPsY9uNAQ0d7ncboDDXaGxtpe0-jXU7G-Z7-WFxf0W0MGY4ueKr9Mp_ehd56m1x6TV50ep3sm9N9Tr5fLb5d3hS3X6-_XH6-LUzFcCyE1cABRWtbAwCG26bVyEurTa7IJTbABOaHinUCQbSirnRV8waMERI1npNPR93t1G7s0lg_Rr1W2-g2Ot6roJ36v-LdoPpwp0pW1o2UWeDDUWCvfZc3UKswRZ9HVtl1nq0FCYCZ9vHUJ4bdZNOoNi4Zm63zNkxJCSgRZVVl4sWRaGJIKdruzywM1CHNg67KaSon1SHN_OPdvyv85Z_iy4T3J8kh-H6X7VetNj87t7aKlwi1kBU-AT5UqwU</recordid><startdate>20070228</startdate><enddate>20070228</enddate><creator>Zhu, Bao-He</creator><creator>Zhan, Wen-Hua</creator><creator>Li, Zheng-Rong</creator><creator>Wang, Zhao</creator><creator>He, Yu-Long</creator><creator>Peng, Jun-Sheng</creator><creator>Cai, Shi-Rong</creator><creator>Ma, Jin-Ping</creator><creator>Zhang, Chang-Hua</creator><general>Department of Gastrointestinal & Pancreatic Surgery, First Affiliated Hospital, Sun Yat-Sen University</general><general>Gastric Center of Sun Yat-Sen University, Guangzhou 510080,Guangdong Province, China</general><general>Baishideng Publishing Group Co., Limited</general><scope>2RA</scope><scope>92L</scope><scope>CQIGP</scope><scope>W91</scope><scope>~WA</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><scope>2B.</scope><scope>4A8</scope><scope>92I</scope><scope>93N</scope><scope>PSX</scope><scope>TCJ</scope><scope>5PM</scope></search><sort><creationdate>20070228</creationdate><title>（-）-Epigallocatechin-3-gallate inhibits growth of gastric cancer by reducing VEGF production and angiogenesis</title><author>Zhu, Bao-He ; 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METHODS： Heterotopic tumors were induced by subcutaneously injection of SGC-7901 cells in nude mice. Tumor growth was measured by calipers in two dimensions. Tumor angiogenesis was determined with tumor microvessel density （MVD） by immunohistology. Vascular endothelial growth factor （VEGF） protein level and activation of signal transducer and activator of transcription 3 （Star3） were examined by Western blotting. VEGF mRNA expression was determined by RT-PCR and VEGF release in tumor culture medium by ELISA. VEGF-induced cell proliferation was studied by MTT assay, cell migration by gelatin modified Boyden chamber （Transwell） and in vitro angiogenesis by endothelial tube formation in Matrigel.
RESULTS： Intraperitoneal injection of EGCG inhibited the growth of gastric cancer by 60.4%. MVD in tumor tissues treated with EGCG was markedly reduced. EGCG treatment reduced VEGF protein level in vitro and in vivo. Secretion and mRNA expression of VEGF in tumor cells were also suppressed by EGCG in a dose-dependent manner. This inhibitory effect was associated with reduced activation of Star3, but EGCG treatment did not change the total Star3 expression. EGCG also inhibited VEGF-induced endothelial cell proliferation, migration and tube formation.
CONCLUSION： EGCG inhibits the growth of gastric cancer by reducing VEGF production and angiogenesis, and is a promising candidate for anti-angiogenic treatment of gastric cancer.</abstract><cop>United States</cop><pub>Department of Gastrointestinal & Pancreatic Surgery, First Affiliated Hospital, Sun Yat-Sen University</pub><pmid>17451194</pmid><doi>10.3748/wjg.v13.i8.1162</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; PubMed Central; Alma/SFX Local Collection |
| subjects | Animals Anticarcinogenic Agents - pharmacology Anticarcinogenic Agents - therapeutic use Carcinoma - drug therapy Carcinoma - pathology Catechin - analogs & derivatives Catechin - pharmacology Catechin - therapeutic use Cell Line, Tumor Cell Movement - drug effects Cell Proliferation - drug effects Endothelial Cells - drug effects Female Gastric Cancer Gene Expression Regulation, Neoplastic Humans Mice Mice, Inbred BALB C Mice, Nude Neovascularization, Pathologic - drug therapy STAT3 Transcription Factor - drug effects Stomach Neoplasms - drug therapy Stomach Neoplasms - pathology Vascular Endothelial Growth Factor A - drug effects VEGF生成 Xenograft Model Antitumor Assays 抑制作用 肿瘤生长 血管发生 表没食子儿茶素-3-没食子酸酯 |
| title | （-）-Epigallocatechin-3-gallate inhibits growth of gastric cancer by reducing VEGF production and angiogenesis |
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