Rosiglitazone enhances fluorouracil-induced apoptosis of HT-29 cells by activating peroxisome proliferator-activated receptor γ
AIM： To examine whether and how rosiglitazone enhances apoptosis induced by fluorouracil in human colon cancer （HT-29） cells. METHODS： Human colon cancer HT-29 cells were cultured in vitro and treated with fluorouracil and/or rosiglitazone. Proliferation and growth of HT-29 cells were evaluated by M...
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| Veröffentlicht in: | World journal of gastroenterology : WJG 2007-03, Vol.13 (10), p.1534-1540 |
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| container_title | World journal of gastroenterology : WJG |
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| creator | Zhang, Yan-Qin Tang, Xiao-Qing Sun, Li Dong, Lin Qin, Yong Liu, Hua-Qing Xia, Hong Cao, Jian-Guo |
| description | AIM： To examine whether and how rosiglitazone enhances apoptosis induced by fluorouracil in human colon cancer （HT-29） cells. METHODS： Human colon cancer HT-29 cells were cultured in vitro and treated with fluorouracil and/or rosiglitazone. Proliferation and growth of HT-29 cells were evaluated by MTF assay and trypan blue exclusion methods, respectively. The apoptosis of HT-29 cells was determined by acridine orange/ethidium bromide staining and flow cytometry using PI fluorescence staining. The expressions of peroxisome proliferator-activated receptor γ （PPARγ）, Bcl-2 and Bax in HT-29 cells were analyzed by Western blot. RESULTS： Although rosiglitazone at the concentration below 30 μmol/L for 72 h exerted almost no inhibitory effect on proliferation and growth of HT-29 cells, it could significantly enhance fluorouracil-induced HT-29 cell proliferation and growth inhibition. Furthermore, 10 μmol/L rosilitazone did not induce apoptosis of HT-29 cells but dramatically enhanced fluorouracil-induced apoptosis of HT-29 cells. However, rosiglitazone did not improve apoptosis induced by fluorouracil in HT-29 cells pretreated with GW9662, a PPARγ antagonist. Meanwhile, the expression of Bax and PPAR7 was upregulated, while the expression of Bcl-2 was down regulated in HT-29 cells treated with rosiglitazone in a time-dependent manner. However, the effect of rosiglitazone on Bcl-2 and Bax was blocked or diminished in the presence of GW9662. CONCLUSION： Rosiglitazone enhances fluorouracilinduced apoptosis of HT-29 cells by activating PPARγ. |
| doi_str_mv | 10.3748/wjg.v13.i10.1534 |
| format | Article |
| fullrecord | <record><control><sourceid>wanfang_jour_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4146895</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><cqvip_id>24392301</cqvip_id><wanfj_id>wjg200710009</wanfj_id><sourcerecordid>wjg200710009</sourcerecordid><originalsourceid>FETCH-LOGICAL-c450t-c33bbdd38dd5774bbf644dfff57e5dfcb5278745922fad31ea46d76c704a83b53</originalsourceid><addsrcrecordid>eNpVkVtrFDEYhoModq3eeyVBvJ1tjpOZG0GKWqFQKO11yOQwmzWbjMnstvXK_-T_6G9qll08XAWS53vz8T4AvMVoSQXrzu7W43KH6dLXC8wpewYWhOC-IR1Dz8ECIySanhJxAl6VskaIUMrJS3CCBWsxY3wBfl2n4sfgZ_UzRQttXKmobYEubFNO26y0D42PZqutgWpK01z5ApODFzcN6aG2IRQ4PEClZ79Ts48jnGxO976kjYVTTsE7m9WccnNEalC22takDB9_vwYvnArFvjmep-D2y-eb84vm8urrt_NPl41mHM2NpnQYjKGdMVwINgyuZcw457iw3Dg9cCI6wXhPiFOGYqtYa0SrBWKqowOnp-DjIXfaDhtrtI1zVkFO2W9UfpBJefn_S_QrOaadZJi1Xb8P-HAIuFPRqTjKda0n1pVltUBq07Vt1FcMHTCdUynZuj9fYCT30va4rNJklSb30urIu39X-ztwtFSB98fMVYrjj9qxHJT-7nywkjDaE4owfQI0l6T-</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype></control><display><type>article</type><title>Rosiglitazone enhances fluorouracil-induced apoptosis of HT-29 cells by activating peroxisome proliferator-activated receptor γ</title><source>MEDLINE</source><source>PubMed Central</source><source>Alma/SFX Local Collection</source><creator>Zhang, Yan-Qin ; Tang, Xiao-Qing ; Sun, Li ; Dong, Lin ; Qin, Yong ; Liu, Hua-Qing ; Xia, Hong ; Cao, Jian-Guo</creator><creatorcontrib>Zhang, Yan-Qin ; Tang, Xiao-Qing ; Sun, Li ; Dong, Lin ; Qin, Yong ; Liu, Hua-Qing ; Xia, Hong ; Cao, Jian-Guo</creatorcontrib><description>AIM： To examine whether and how rosiglitazone enhances apoptosis induced by fluorouracil in human colon cancer （HT-29） cells. METHODS： Human colon cancer HT-29 cells were cultured in vitro and treated with fluorouracil and/or rosiglitazone. Proliferation and growth of HT-29 cells were evaluated by MTF assay and trypan blue exclusion methods, respectively. The apoptosis of HT-29 cells was determined by acridine orange/ethidium bromide staining and flow cytometry using PI fluorescence staining. The expressions of peroxisome proliferator-activated receptor γ （PPARγ）, Bcl-2 and Bax in HT-29 cells were analyzed by Western blot. RESULTS： Although rosiglitazone at the concentration below 30 μmol/L for 72 h exerted almost no inhibitory effect on proliferation and growth of HT-29 cells, it could significantly enhance fluorouracil-induced HT-29 cell proliferation and growth inhibition. Furthermore, 10 μmol/L rosilitazone did not induce apoptosis of HT-29 cells but dramatically enhanced fluorouracil-induced apoptosis of HT-29 cells. However, rosiglitazone did not improve apoptosis induced by fluorouracil in HT-29 cells pretreated with GW9662, a PPARγ antagonist. Meanwhile, the expression of Bax and PPAR7 was upregulated, while the expression of Bcl-2 was down regulated in HT-29 cells treated with rosiglitazone in a time-dependent manner. However, the effect of rosiglitazone on Bcl-2 and Bax was blocked or diminished in the presence of GW9662. CONCLUSION： Rosiglitazone enhances fluorouracilinduced apoptosis of HT-29 cells by activating PPARγ.</description><identifier>ISSN: 1007-9327</identifier><identifier>EISSN: 2219-2840</identifier><identifier>DOI: 10.3748/wjg.v13.i10.1534</identifier><identifier>PMID: 17461445</identifier><language>eng</language><publisher>United States: Cancer Research Institute of Nanhua University, Hengyang 421001, Hunan Province, China%Department of Pharmacology, School of Pharmaceutical Sciences, Central South University, Changsha 410078, Hunan Province, China</publisher><subject>Anilides - pharmacology ; Antimetabolites, Antineoplastic - pharmacology ; Apoptosis - drug effects ; bcl-2-Associated X Protein - genetics ; bcl-2-Associated X Protein - physiology ; Cell Line, Tumor ; Cell Proliferation - drug effects ; Colonic Neoplasms - pathology ; Colonic Neoplasms - physiopathology ; Colorectal Cancer ; Fluorouracil - pharmacology ; Gene Expression Regulation - drug effects ; HT-29细胞 ; Humans ; Hypoglycemic Agents - pharmacology ; PPAR gamma - antagonists & inhibitors ; PPAR gamma - genetics ; PPAR gamma - physiology ; PPARγ ; Proto-Oncogene Proteins c-bcl-2 - genetics ; Proto-Oncogene Proteins c-bcl-2 - physiology ; Rosiglitazone ; Thiazolidinediones - pharmacology ; 促进作用 ; 氟尿嘧啶 ; 结肠癌 ; 罗格列酮 ; 诱发凋亡</subject><ispartof>World journal of gastroenterology : WJG, 2007-03, Vol.13 (10), p.1534-1540</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-c450t-c33bbdd38dd5774bbf644dfff57e5dfcb5278745922fad31ea46d76c704a83b53</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/PMC4146895/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4146895/$$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/17461445$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, Yan-Qin</creatorcontrib><creatorcontrib>Tang, Xiao-Qing</creatorcontrib><creatorcontrib>Sun, Li</creatorcontrib><creatorcontrib>Dong, Lin</creatorcontrib><creatorcontrib>Qin, Yong</creatorcontrib><creatorcontrib>Liu, Hua-Qing</creatorcontrib><creatorcontrib>Xia, Hong</creatorcontrib><creatorcontrib>Cao, Jian-Guo</creatorcontrib><title>Rosiglitazone enhances fluorouracil-induced apoptosis of HT-29 cells by activating peroxisome proliferator-activated receptor γ</title><title>World journal of gastroenterology : WJG</title><addtitle>World Journal of Gastroenterology</addtitle><description>AIM： To examine whether and how rosiglitazone enhances apoptosis induced by fluorouracil in human colon cancer （HT-29） cells. METHODS： Human colon cancer HT-29 cells were cultured in vitro and treated with fluorouracil and/or rosiglitazone. Proliferation and growth of HT-29 cells were evaluated by MTF assay and trypan blue exclusion methods, respectively. The apoptosis of HT-29 cells was determined by acridine orange/ethidium bromide staining and flow cytometry using PI fluorescence staining. The expressions of peroxisome proliferator-activated receptor γ （PPARγ）, Bcl-2 and Bax in HT-29 cells were analyzed by Western blot. RESULTS： Although rosiglitazone at the concentration below 30 μmol/L for 72 h exerted almost no inhibitory effect on proliferation and growth of HT-29 cells, it could significantly enhance fluorouracil-induced HT-29 cell proliferation and growth inhibition. Furthermore, 10 μmol/L rosilitazone did not induce apoptosis of HT-29 cells but dramatically enhanced fluorouracil-induced apoptosis of HT-29 cells. However, rosiglitazone did not improve apoptosis induced by fluorouracil in HT-29 cells pretreated with GW9662, a PPARγ antagonist. Meanwhile, the expression of Bax and PPAR7 was upregulated, while the expression of Bcl-2 was down regulated in HT-29 cells treated with rosiglitazone in a time-dependent manner. However, the effect of rosiglitazone on Bcl-2 and Bax was blocked or diminished in the presence of GW9662. CONCLUSION： Rosiglitazone enhances fluorouracilinduced apoptosis of HT-29 cells by activating PPARγ.</description><subject>Anilides - pharmacology</subject><subject>Antimetabolites, Antineoplastic - pharmacology</subject><subject>Apoptosis - drug effects</subject><subject>bcl-2-Associated X Protein - genetics</subject><subject>bcl-2-Associated X Protein - physiology</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation - drug effects</subject><subject>Colonic Neoplasms - pathology</subject><subject>Colonic Neoplasms - physiopathology</subject><subject>Colorectal Cancer</subject><subject>Fluorouracil - pharmacology</subject><subject>Gene Expression Regulation - drug effects</subject><subject>HT-29细胞</subject><subject>Humans</subject><subject>Hypoglycemic Agents - pharmacology</subject><subject>PPAR gamma - antagonists & inhibitors</subject><subject>PPAR gamma - genetics</subject><subject>PPAR gamma - physiology</subject><subject>PPARγ</subject><subject>Proto-Oncogene Proteins c-bcl-2 - genetics</subject><subject>Proto-Oncogene Proteins c-bcl-2 - physiology</subject><subject>Rosiglitazone</subject><subject>Thiazolidinediones - pharmacology</subject><subject>促进作用</subject><subject>氟尿嘧啶</subject><subject>结肠癌</subject><subject>罗格列酮</subject><subject>诱发凋亡</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>eNpVkVtrFDEYhoModq3eeyVBvJ1tjpOZG0GKWqFQKO11yOQwmzWbjMnstvXK_-T_6G9qll08XAWS53vz8T4AvMVoSQXrzu7W43KH6dLXC8wpewYWhOC-IR1Dz8ECIySanhJxAl6VskaIUMrJS3CCBWsxY3wBfl2n4sfgZ_UzRQttXKmobYEubFNO26y0D42PZqutgWpK01z5ApODFzcN6aG2IRQ4PEClZ79Ts48jnGxO976kjYVTTsE7m9WccnNEalC22takDB9_vwYvnArFvjmep-D2y-eb84vm8urrt_NPl41mHM2NpnQYjKGdMVwINgyuZcw457iw3Dg9cCI6wXhPiFOGYqtYa0SrBWKqowOnp-DjIXfaDhtrtI1zVkFO2W9UfpBJefn_S_QrOaadZJi1Xb8P-HAIuFPRqTjKda0n1pVltUBq07Vt1FcMHTCdUynZuj9fYCT30va4rNJklSb30urIu39X-ztwtFSB98fMVYrjj9qxHJT-7nywkjDaE4owfQI0l6T-</recordid><startdate>20070314</startdate><enddate>20070314</enddate><creator>Zhang, Yan-Qin</creator><creator>Tang, Xiao-Qing</creator><creator>Sun, Li</creator><creator>Dong, Lin</creator><creator>Qin, Yong</creator><creator>Liu, Hua-Qing</creator><creator>Xia, Hong</creator><creator>Cao, Jian-Guo</creator><general>Cancer Research Institute of Nanhua University, Hengyang 421001, Hunan Province, China%Department of Pharmacology, School of Pharmaceutical Sciences, Central South University, Changsha 410078, Hunan 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>2B.</scope><scope>4A8</scope><scope>92I</scope><scope>93N</scope><scope>PSX</scope><scope>TCJ</scope><scope>5PM</scope></search><sort><creationdate>20070314</creationdate><title>Rosiglitazone enhances fluorouracil-induced apoptosis of HT-29 cells by activating peroxisome proliferator-activated receptor γ</title><author>Zhang, Yan-Qin ; 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METHODS： Human colon cancer HT-29 cells were cultured in vitro and treated with fluorouracil and/or rosiglitazone. Proliferation and growth of HT-29 cells were evaluated by MTF assay and trypan blue exclusion methods, respectively. The apoptosis of HT-29 cells was determined by acridine orange/ethidium bromide staining and flow cytometry using PI fluorescence staining. The expressions of peroxisome proliferator-activated receptor γ （PPARγ）, Bcl-2 and Bax in HT-29 cells were analyzed by Western blot. RESULTS： Although rosiglitazone at the concentration below 30 μmol/L for 72 h exerted almost no inhibitory effect on proliferation and growth of HT-29 cells, it could significantly enhance fluorouracil-induced HT-29 cell proliferation and growth inhibition. Furthermore, 10 μmol/L rosilitazone did not induce apoptosis of HT-29 cells but dramatically enhanced fluorouracil-induced apoptosis of HT-29 cells. However, rosiglitazone did not improve apoptosis induced by fluorouracil in HT-29 cells pretreated with GW9662, a PPARγ antagonist. Meanwhile, the expression of Bax and PPAR7 was upregulated, while the expression of Bcl-2 was down regulated in HT-29 cells treated with rosiglitazone in a time-dependent manner. However, the effect of rosiglitazone on Bcl-2 and Bax was blocked or diminished in the presence of GW9662. CONCLUSION： Rosiglitazone enhances fluorouracilinduced apoptosis of HT-29 cells by activating PPARγ.</abstract><cop>United States</cop><pub>Cancer Research Institute of Nanhua University, Hengyang 421001, Hunan Province, China%Department of Pharmacology, School of Pharmaceutical Sciences, Central South University, Changsha 410078, Hunan Province, China</pub><pmid>17461445</pmid><doi>10.3748/wjg.v13.i10.1534</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| identifier | ISSN: 1007-9327 |
| ispartof | World journal of gastroenterology : WJG, 2007-03, Vol.13 (10), p.1534-1540 |
| issn | 1007-9327 2219-2840 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4146895 |
| source | MEDLINE; PubMed Central; Alma/SFX Local Collection |
| subjects | Anilides - pharmacology Antimetabolites, Antineoplastic - pharmacology Apoptosis - drug effects bcl-2-Associated X Protein - genetics bcl-2-Associated X Protein - physiology Cell Line, Tumor Cell Proliferation - drug effects Colonic Neoplasms - pathology Colonic Neoplasms - physiopathology Colorectal Cancer Fluorouracil - pharmacology Gene Expression Regulation - drug effects HT-29细胞 Humans Hypoglycemic Agents - pharmacology PPAR gamma - antagonists & inhibitors PPAR gamma - genetics PPAR gamma - physiology PPARγ Proto-Oncogene Proteins c-bcl-2 - genetics Proto-Oncogene Proteins c-bcl-2 - physiology Rosiglitazone Thiazolidinediones - pharmacology 促进作用 氟尿嘧啶 结肠癌 罗格列酮 诱发凋亡 |
| title | Rosiglitazone enhances fluorouracil-induced apoptosis of HT-29 cells by activating peroxisome proliferator-activated receptor γ |
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