Cytochalasin D,a tropical fungal metabolite,inhibits CT26 tumor growth and angiogenesis
<正>Objective:To investigate whether eytochalasin D can induce antitumor activities in a tumor model.Methods:Murine CT26 colorectal carcinoma cells were cultured hi vitro and cytochalasin D was used as a cytotoxic agent to detect its capabilities of inhibiting CT26 cell proliferation an...
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Veröffentlicht in: | Asian Pacific journal of tropical medicine 2012-03, Vol.5 (3), p.169-174 |
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creator | Huang, Feng-Ying Li, Yue-Nan Mei, Wen-Li Dai, Hao-Fu Zhou, Peng Tan, Guang-Hong |
description | <正>Objective:To investigate whether eytochalasin D can induce antitumor activities in a tumor model.Methods:Murine CT26 colorectal carcinoma cells were cultured hi vitro and cytochalasin D was used as a cytotoxic agent to detect its capabilities of inhibiting CT26 cell proliferation and inducing cell apoptosis by MTT and a TUNEL-based apoptosis assay.Murine CT26 tumor model was established to observe the tumor growth and survival time.Tumor tissues were used to detect the mierovessel density by immunohistochemistry.In addition,alginate encapsulated tumor cell assay was used to quantify the tumor angiogenesis in vivo.Results:Cytochalasin D inhibited CT26 tumor cell proliferation in lime and dose dependent manner and induced signiflcanl CT26 cell apoptosis,which almost reached the level induced by the positive control nuclease.The optimum effective dose of cytochalasin D for in vivo therapy was about 50 mg/kg.Cytochalasin D in vivo treatment significandy inhibited tumor growth and prolonged the survival times in CT26 tumor-bearing mice.The results of immunohistochemistry analysis and alginate encapsulation assay indicated that the cytochalasin D could effectively inhibited tumor angiogenesis. Conclusions:Cytochalasin D inhibits CT26 tumor growth potentially through inhibition of cell proliferation,induction of cell apoptosis and suppression of tumor angiogenesis. |
doi_str_mv | 10.1016/S1995-7645(12)60019-4 |
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fullrecord | <record><control><sourceid>wanfang_jour_proqu</sourceid><recordid>TN_cdi_wanfang_journals_yrdyyzz_e201203001</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><cqvip_id>1003037077</cqvip_id><wanfj_id>yrdyyzz_e201203001</wanfj_id><els_id>S1995764512600194</els_id><sourcerecordid>yrdyyzz_e201203001</sourcerecordid><originalsourceid>FETCH-LOGICAL-c606t-28e3ab366d84498ce0d8985f55d3b78b779924af75d18eca8fa09e9cb6785d3c3</originalsourceid><addsrcrecordid>eNqFkUtv1DAUhS0EoqPSnwCKxIKCGvDb8QqhKS-pEguKWFqO42RcJfbUdqjSX19PZyg7asm6m-_ec3QOAC8RfI8g4h9-IilZLThlpwi_5RAiWdMnYIUJwzVFlD8FqwfkCJykdAXLI1hKQZ6DI4wJZELIFfi9XnIwGz3q5Hx1fqarHMPWGT1W_eyHMiabdRtGl-2Z8xvXupyq9SXmVZ6nEKshhpu8qbTvyh9cGKy3yaUX4Fmvx2RPDvMY_Pry-XL9rb748fX7-tNFbTjkucaNJbolnHcNpbIxFnaNbFjPWEda0bTFo8RU94J1qLFGN72G0krTctEUxJBj8G5_90b7vhhQV2GOviiqJXbLcnurLIYIQ1IyKvCbPbyN4Xq2KavJJWPHUXsb5qQkhhgLSXkhT_9LIs4hJYRJ-jhabjKBsIAFZXvUxJBStL3aRjfpuBRI7YpV98WqXWsKYXVfrNpJvDpIzO1ku4etvzUW4OMesCXqP85GlYyz3tjORWuy6oJ7VOL1wdom-OHalST_eSvpEQGFIHe76bye</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1022571270</pqid></control><display><type>article</type><title>Cytochalasin D,a tropical fungal metabolite,inhibits CT26 tumor growth and angiogenesis</title><source>MEDLINE</source><source>Elsevier ScienceDirect Journals Complete</source><source>EZB-FREE-00999 freely available EZB journals</source><creator>Huang, Feng-Ying ; Li, Yue-Nan ; Mei, Wen-Li ; Dai, Hao-Fu ; Zhou, Peng ; Tan, Guang-Hong</creator><creatorcontrib>Huang, Feng-Ying ; Li, Yue-Nan ; Mei, Wen-Li ; Dai, Hao-Fu ; Zhou, Peng ; Tan, Guang-Hong</creatorcontrib><description>&lt;正&gt;Objective:To investigate whether eytochalasin D can induce antitumor activities in a tumor model.Methods:Murine CT26 colorectal carcinoma cells were cultured hi vitro and cytochalasin D was used as a cytotoxic agent to detect its capabilities of inhibiting CT26 cell proliferation and inducing cell apoptosis by MTT and a TUNEL-based apoptosis assay.Murine CT26 tumor model was established to observe the tumor growth and survival time.Tumor tissues were used to detect the mierovessel density by immunohistochemistry.In addition,alginate encapsulated tumor cell assay was used to quantify the tumor angiogenesis in vivo.Results:Cytochalasin D inhibited CT26 tumor cell proliferation in lime and dose dependent manner and induced signiflcanl CT26 cell apoptosis,which almost reached the level induced by the positive control nuclease.The optimum effective dose of cytochalasin D for in vivo therapy was about 50 mg/kg.Cytochalasin D in vivo treatment significandy inhibited tumor growth and prolonged the survival times in CT26 tumor-bearing mice.The results of immunohistochemistry analysis and alginate encapsulation assay indicated that the cytochalasin D could effectively inhibited tumor angiogenesis. Conclusions:Cytochalasin D inhibits CT26 tumor growth potentially through inhibition of cell proliferation,induction of cell apoptosis and suppression of tumor angiogenesis.</description><identifier>ISSN: 1995-7645</identifier><identifier>EISSN: 2352-4146</identifier><identifier>DOI: 10.1016/S1995-7645(12)60019-4</identifier><identifier>PMID: 22305779</identifier><language>eng</language><publisher>India: Elsevier B.V</publisher><subject>Alginic acid ; Angiogenesis ; Angiogenesis Inhibitors - administration & dosage ; Angiogenesis Inhibitors - pharmacology ; Animal models ; Animals ; Antineoplastic Agents - administration & dosage ; Antineoplastic Agents - pharmacology ; Antitumor activity ; Apoptosis ; Apoptosis - drug effects ; carcinoma ; Cell proliferation ; Cell Proliferation - drug effects ; colorectal ; Colorectal carcinoma ; Colorectal Neoplasms - blood supply ; Colorectal Neoplasms - drug therapy ; CT26 ; CT26 colorectal carcinoma ; Cytochalasin ; Cytochalasin D ; Cytochalasin D - administration & dosage ; Cytochalasin D - pharmacology ; Cytotoxic agents ; Dose-Response Relationship, Drug ; Encapsulation ; Immunohistochemistry ; In Situ Nick-End Labeling ; Metabolites ; Mice ; Microvessels - drug effects ; Neovascularization, Pathologic - prevention & control ; Nuclease ; Tumor ; Tumor angiogenesis ; Tumor cells ; Tumor Cells, Cultured ; Tumors</subject><ispartof>Asian Pacific journal of tropical medicine, 2012-03, Vol.5 (3), p.169-174</ispartof><rights>2012 Hainan Medical College</rights><rights>Copyright © 2012 Hainan Medical College. Published by Elsevier B.V. All rights reserved.</rights><rights>Copyright © Wanfang Data Co. Ltd. All Rights Reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c606t-28e3ab366d84498ce0d8985f55d3b78b779924af75d18eca8fa09e9cb6785d3c3</citedby><cites>FETCH-LOGICAL-c606t-28e3ab366d84498ce0d8985f55d3b78b779924af75d18eca8fa09e9cb6785d3c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Uhttp://image.cqvip.com/vip1000/qk/71792X/71792X.jpg</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/S1995-7645(12)60019-4$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22305779$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Huang, Feng-Ying</creatorcontrib><creatorcontrib>Li, Yue-Nan</creatorcontrib><creatorcontrib>Mei, Wen-Li</creatorcontrib><creatorcontrib>Dai, Hao-Fu</creatorcontrib><creatorcontrib>Zhou, Peng</creatorcontrib><creatorcontrib>Tan, Guang-Hong</creatorcontrib><title>Cytochalasin D,a tropical fungal metabolite,inhibits CT26 tumor growth and angiogenesis</title><title>Asian Pacific journal of tropical medicine</title><addtitle>Asian Pacific Journal of Tropical Medicine</addtitle><description>&lt;正&gt;Objective:To investigate whether eytochalasin D can induce antitumor activities in a tumor model.Methods:Murine CT26 colorectal carcinoma cells were cultured hi vitro and cytochalasin D was used as a cytotoxic agent to detect its capabilities of inhibiting CT26 cell proliferation and inducing cell apoptosis by MTT and a TUNEL-based apoptosis assay.Murine CT26 tumor model was established to observe the tumor growth and survival time.Tumor tissues were used to detect the mierovessel density by immunohistochemistry.In addition,alginate encapsulated tumor cell assay was used to quantify the tumor angiogenesis in vivo.Results:Cytochalasin D inhibited CT26 tumor cell proliferation in lime and dose dependent manner and induced signiflcanl CT26 cell apoptosis,which almost reached the level induced by the positive control nuclease.The optimum effective dose of cytochalasin D for in vivo therapy was about 50 mg/kg.Cytochalasin D in vivo treatment significandy inhibited tumor growth and prolonged the survival times in CT26 tumor-bearing mice.The results of immunohistochemistry analysis and alginate encapsulation assay indicated that the cytochalasin D could effectively inhibited tumor angiogenesis. Conclusions:Cytochalasin D inhibits CT26 tumor growth potentially through inhibition of cell proliferation,induction of cell apoptosis and suppression of tumor angiogenesis.</description><subject>Alginic acid</subject><subject>Angiogenesis</subject><subject>Angiogenesis Inhibitors - administration & dosage</subject><subject>Angiogenesis Inhibitors - pharmacology</subject><subject>Animal models</subject><subject>Animals</subject><subject>Antineoplastic Agents - administration & dosage</subject><subject>Antineoplastic Agents - pharmacology</subject><subject>Antitumor activity</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>carcinoma</subject><subject>Cell proliferation</subject><subject>Cell Proliferation - drug effects</subject><subject>colorectal</subject><subject>Colorectal carcinoma</subject><subject>Colorectal Neoplasms - blood supply</subject><subject>Colorectal Neoplasms - drug therapy</subject><subject>CT26</subject><subject>CT26 colorectal carcinoma</subject><subject>Cytochalasin</subject><subject>Cytochalasin D</subject><subject>Cytochalasin D - administration & dosage</subject><subject>Cytochalasin D - pharmacology</subject><subject>Cytotoxic agents</subject><subject>Dose-Response Relationship, Drug</subject><subject>Encapsulation</subject><subject>Immunohistochemistry</subject><subject>In Situ Nick-End Labeling</subject><subject>Metabolites</subject><subject>Mice</subject><subject>Microvessels - drug effects</subject><subject>Neovascularization, Pathologic - prevention & control</subject><subject>Nuclease</subject><subject>Tumor</subject><subject>Tumor angiogenesis</subject><subject>Tumor cells</subject><subject>Tumor Cells, Cultured</subject><subject>Tumors</subject><issn>1995-7645</issn><issn>2352-4146</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkUtv1DAUhS0EoqPSnwCKxIKCGvDb8QqhKS-pEguKWFqO42RcJfbUdqjSX19PZyg7asm6m-_ec3QOAC8RfI8g4h9-IilZLThlpwi_5RAiWdMnYIUJwzVFlD8FqwfkCJykdAXLI1hKQZ6DI4wJZELIFfi9XnIwGz3q5Hx1fqarHMPWGT1W_eyHMiabdRtGl-2Z8xvXupyq9SXmVZ6nEKshhpu8qbTvyh9cGKy3yaUX4Fmvx2RPDvMY_Pry-XL9rb748fX7-tNFbTjkucaNJbolnHcNpbIxFnaNbFjPWEda0bTFo8RU94J1qLFGN72G0krTctEUxJBj8G5_90b7vhhQV2GOviiqJXbLcnurLIYIQ1IyKvCbPbyN4Xq2KavJJWPHUXsb5qQkhhgLSXkhT_9LIs4hJYRJ-jhabjKBsIAFZXvUxJBStL3aRjfpuBRI7YpV98WqXWsKYXVfrNpJvDpIzO1ku4etvzUW4OMesCXqP85GlYyz3tjORWuy6oJ7VOL1wdom-OHalST_eSvpEQGFIHe76bye</recordid><startdate>20120301</startdate><enddate>20120301</enddate><creator>Huang, Feng-Ying</creator><creator>Li, Yue-Nan</creator><creator>Mei, Wen-Li</creator><creator>Dai, Hao-Fu</creator><creator>Zhou, Peng</creator><creator>Tan, Guang-Hong</creator><general>Elsevier B.V</general><general>Agriculture College, Hainan University, Haikou, China%Hainan Provincial Key Laboratory of Tropical Medicine, Hainan Medical College, Haikou, China</general><scope>2RA</scope><scope>92L</scope><scope>CQIGP</scope><scope>W91</scope><scope>~WA</scope><scope>6I.</scope><scope>AAFTH</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>M7N</scope><scope>C1K</scope><scope>F1W</scope><scope>H95</scope><scope>H97</scope><scope>L.G</scope><scope>7X8</scope><scope>2B.</scope><scope>4A8</scope><scope>92I</scope><scope>93N</scope><scope>PSX</scope><scope>TCJ</scope></search><sort><creationdate>20120301</creationdate><title>Cytochalasin D,a tropical fungal metabolite,inhibits CT26 tumor growth and angiogenesis</title><author>Huang, Feng-Ying ; Li, Yue-Nan ; Mei, Wen-Li ; Dai, Hao-Fu ; Zhou, Peng ; Tan, Guang-Hong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c606t-28e3ab366d84498ce0d8985f55d3b78b779924af75d18eca8fa09e9cb6785d3c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Alginic acid</topic><topic>Angiogenesis</topic><topic>Angiogenesis Inhibitors - administration & dosage</topic><topic>Angiogenesis Inhibitors - pharmacology</topic><topic>Animal models</topic><topic>Animals</topic><topic>Antineoplastic Agents - administration & dosage</topic><topic>Antineoplastic Agents - pharmacology</topic><topic>Antitumor activity</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>carcinoma</topic><topic>Cell proliferation</topic><topic>Cell Proliferation - drug effects</topic><topic>colorectal</topic><topic>Colorectal carcinoma</topic><topic>Colorectal Neoplasms - blood supply</topic><topic>Colorectal Neoplasms - drug therapy</topic><topic>CT26</topic><topic>CT26 colorectal carcinoma</topic><topic>Cytochalasin</topic><topic>Cytochalasin D</topic><topic>Cytochalasin D - administration & dosage</topic><topic>Cytochalasin D - pharmacology</topic><topic>Cytotoxic agents</topic><topic>Dose-Response Relationship, Drug</topic><topic>Encapsulation</topic><topic>Immunohistochemistry</topic><topic>In Situ Nick-End Labeling</topic><topic>Metabolites</topic><topic>Mice</topic><topic>Microvessels - drug effects</topic><topic>Neovascularization, Pathologic - prevention & control</topic><topic>Nuclease</topic><topic>Tumor</topic><topic>Tumor angiogenesis</topic><topic>Tumor cells</topic><topic>Tumor Cells, Cultured</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Huang, Feng-Ying</creatorcontrib><creatorcontrib>Li, Yue-Nan</creatorcontrib><creatorcontrib>Mei, Wen-Li</creatorcontrib><creatorcontrib>Dai, Hao-Fu</creatorcontrib><creatorcontrib>Zhou, Peng</creatorcontrib><creatorcontrib>Tan, Guang-Hong</creatorcontrib><collection>中文科技期刊数据库</collection><collection>中文科技期刊数据库-CALIS站点</collection><collection>中文科技期刊数据库-7.0平台</collection><collection>中文科技期刊数据库-医药卫生</collection><collection>中文科技期刊数据库- 镜像站点</collection><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ASFA: Aquatic Sciences and Fisheries Abstracts</collection><collection>Aquatic Science & Fisheries Abstracts (ASFA) 1: Biological Sciences & Living Resources</collection><collection>Aquatic Science & Fisheries Abstracts (ASFA) 3: Aquatic Pollution & Environmental Quality</collection><collection>Aquatic Science & Fisheries Abstracts (ASFA) Professional</collection><collection>MEDLINE - Academic</collection><collection>Wanfang Data Journals - Hong Kong</collection><collection>WANFANG Data Centre</collection><collection>Wanfang Data Journals</collection><collection>万方数据期刊 - 香港版</collection><collection>China Online Journals (COJ)</collection><collection>China Online Journals (COJ)</collection><jtitle>Asian Pacific journal of tropical medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Huang, Feng-Ying</au><au>Li, Yue-Nan</au><au>Mei, Wen-Li</au><au>Dai, Hao-Fu</au><au>Zhou, Peng</au><au>Tan, Guang-Hong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cytochalasin D,a tropical fungal metabolite,inhibits CT26 tumor growth and angiogenesis</atitle><jtitle>Asian Pacific journal of tropical medicine</jtitle><addtitle>Asian Pacific Journal of Tropical Medicine</addtitle><date>2012-03-01</date><risdate>2012</risdate><volume>5</volume><issue>3</issue><spage>169</spage><epage>174</epage><pages>169-174</pages><issn>1995-7645</issn><eissn>2352-4146</eissn><abstract>&lt;正&gt;Objective:To investigate whether eytochalasin D can induce antitumor activities in a tumor model.Methods:Murine CT26 colorectal carcinoma cells were cultured hi vitro and cytochalasin D was used as a cytotoxic agent to detect its capabilities of inhibiting CT26 cell proliferation and inducing cell apoptosis by MTT and a TUNEL-based apoptosis assay.Murine CT26 tumor model was established to observe the tumor growth and survival time.Tumor tissues were used to detect the mierovessel density by immunohistochemistry.In addition,alginate encapsulated tumor cell assay was used to quantify the tumor angiogenesis in vivo.Results:Cytochalasin D inhibited CT26 tumor cell proliferation in lime and dose dependent manner and induced signiflcanl CT26 cell apoptosis,which almost reached the level induced by the positive control nuclease.The optimum effective dose of cytochalasin D for in vivo therapy was about 50 mg/kg.Cytochalasin D in vivo treatment significandy inhibited tumor growth and prolonged the survival times in CT26 tumor-bearing mice.The results of immunohistochemistry analysis and alginate encapsulation assay indicated that the cytochalasin D could effectively inhibited tumor angiogenesis. Conclusions:Cytochalasin D inhibits CT26 tumor growth potentially through inhibition of cell proliferation,induction of cell apoptosis and suppression of tumor angiogenesis.</abstract><cop>India</cop><pub>Elsevier B.V</pub><pmid>22305779</pmid><doi>10.1016/S1995-7645(12)60019-4</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Alginic acid Angiogenesis Angiogenesis Inhibitors - administration & dosage Angiogenesis Inhibitors - pharmacology Animal models Animals Antineoplastic Agents - administration & dosage Antineoplastic Agents - pharmacology Antitumor activity Apoptosis Apoptosis - drug effects carcinoma Cell proliferation Cell Proliferation - drug effects colorectal Colorectal carcinoma Colorectal Neoplasms - blood supply Colorectal Neoplasms - drug therapy CT26 CT26 colorectal carcinoma Cytochalasin Cytochalasin D Cytochalasin D - administration & dosage Cytochalasin D - pharmacology Cytotoxic agents Dose-Response Relationship, Drug Encapsulation Immunohistochemistry In Situ Nick-End Labeling Metabolites Mice Microvessels - drug effects Neovascularization, Pathologic - prevention & control Nuclease Tumor Tumor angiogenesis Tumor cells Tumor Cells, Cultured Tumors |
title | Cytochalasin D,a tropical fungal metabolite,inhibits CT26 tumor growth and angiogenesis |
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