Gene expression profile in colon cancer cells with respect to XIAP expression status
Background and aims We observed a marked synergism between peroxisome proliferator-activated receptor gamma (PPARγ) ligands and X-linked inhibitor of apoptosis (XIAP) down-regulation in colon cancer. In the current study, we detected the gene expression profile in HCT116 cells treated with or withou...
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Veröffentlicht in: | International journal of colorectal disease 2009-03, Vol.24 (3), p.245-260 |
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container_title | International journal of colorectal disease |
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creator | Qiao, Liang Li, Gloria H. Y. Dai, Yun Wang, Jide Li, Zesong Zou, Bing Gu, Qing Ma, Juan Pang, R. Lan, Hui Y. Wong, Benjamin C. Y. |
description | Background and aims
We observed a marked synergism between peroxisome proliferator-activated receptor gamma (PPARγ) ligands and X-linked inhibitor of apoptosis (XIAP) down-regulation in colon cancer. In the current study, we detected the gene expression profile in HCT116 cells treated with or without PPARγ ligand troglitazone.
Materials and methods
HCT116-XIAP
+/+
and HCT116-XIAP
−/−
cells were treated with or without 50 μM troglitazone for 48 h. Gene expressions were detected by microarray, and selected genes were validated by reverse-transcriptase polymerase chain reaction (PCR), real-time PCR, and Western blot.
Results
Relative to HCT116-XIAP
+/+
cells, 58 genes were up-regulated and 33 genes down-regulated in HCT116-XIAP
−/−
cells, all by ≥4-fold. These genes could be classified into a wide variety of functional classes, but we focused on those related to angiogenesis, apoptosis, and proliferation. Thus, two pro-apoptotic genes and one pro-proliferation gene were up-regulated in HCT116-XIAP
−/−
cells. Two pro-proliferation genes, one pro-angiogenesis gene, one anti-angiogenesis gene, and one anti-apoptosis gene were down-regulated in HCT116-XIAP
−/−
cells. Relative to HCT116-XIAP
+/+
cells treated with troglitazone, 137 genes were up-regulated, and 31 genes were down-regulated in troglitazone-treated HCT116-XIAP
−/−
cells, all by ≥4-fold. Among the up-regulated genes were two anti-angiogenesis genes, seven pro-apoptosis genes, and six anti-proliferation genes. Among the down-regulated genes were one anti-angiogenesis gene, one pro-angiogenesis gene, one anti-apoptosis gene, one anti-proliferation gene, and two pro-proliferation genes.
Conclusion
Down-regulation of XIAP in HCT116 cells with or without troglitazone treatment was associated with changes of gene expression that favor increased tendency of apoptosis, decreased cell proliferation, and angiogenesis potential. |
doi_str_mv | 10.1007/s00384-008-0566-1 |
format | Article |
fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_20403462</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>20403462</sourcerecordid><originalsourceid>FETCH-LOGICAL-c430t-5742750ad47b3e2e8f96bfdffefc3a05ca81ef93776fde45ea5abc10f15c127a3</originalsourceid><addsrcrecordid>eNp1kMFqGzEQhkVJaJy0D9BLEYHmts2MVlqtj8GkTsCQHBLoTcjyqN2w3nU1uyR5-8rY1KGQk5D0_TM_nxBfEL4jgL1kgLLWBUBdgKmqAj-ICepSFagqdSQmgHZa4NTUJ-KU-QnyvbL6ozjB2oLWxk7Ew5w6kvSyScTc9J3cpD42Lcmmk6Fv80PwXaAkA7Uty-dm-C0zuqEwyKGXP2-v7t-mefDDyJ_EcfQt0-f9eSYef1w_zG6Kxd38dna1KIIuYSiM1coa8CttlyUpquO0WsZVjBRD6cEEXyPFaWltFVekDXnjlwEhogmorC_PxMVubi79ZyQe3LrhbVHfUT-yU6Ch1JXK4Pl_4FM_pi53cworo9BAnSHcQSH1zImi26Rm7dOrQ3Bb327n22XfbuvbYc583Q8el2taHRJ7wRn4tgc8B9_GlG02_I9TCBa10ZlTO47zV_eL0qHh-9v_AqXdmB8</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>216521508</pqid></control><display><type>article</type><title>Gene expression profile in colon cancer cells with respect to XIAP expression status</title><source>MEDLINE</source><source>SpringerLink Journals - AutoHoldings</source><creator>Qiao, Liang ; Li, Gloria H. Y. ; Dai, Yun ; Wang, Jide ; Li, Zesong ; Zou, Bing ; Gu, Qing ; Ma, Juan ; Pang, R. ; Lan, Hui Y. ; Wong, Benjamin C. Y.</creator><creatorcontrib>Qiao, Liang ; Li, Gloria H. Y. ; Dai, Yun ; Wang, Jide ; Li, Zesong ; Zou, Bing ; Gu, Qing ; Ma, Juan ; Pang, R. ; Lan, Hui Y. ; Wong, Benjamin C. Y.</creatorcontrib><description>Background and aims
We observed a marked synergism between peroxisome proliferator-activated receptor gamma (PPARγ) ligands and X-linked inhibitor of apoptosis (XIAP) down-regulation in colon cancer. In the current study, we detected the gene expression profile in HCT116 cells treated with or without PPARγ ligand troglitazone.
Materials and methods
HCT116-XIAP
+/+
and HCT116-XIAP
−/−
cells were treated with or without 50 μM troglitazone for 48 h. Gene expressions were detected by microarray, and selected genes were validated by reverse-transcriptase polymerase chain reaction (PCR), real-time PCR, and Western blot.
Results
Relative to HCT116-XIAP
+/+
cells, 58 genes were up-regulated and 33 genes down-regulated in HCT116-XIAP
−/−
cells, all by ≥4-fold. These genes could be classified into a wide variety of functional classes, but we focused on those related to angiogenesis, apoptosis, and proliferation. Thus, two pro-apoptotic genes and one pro-proliferation gene were up-regulated in HCT116-XIAP
−/−
cells. Two pro-proliferation genes, one pro-angiogenesis gene, one anti-angiogenesis gene, and one anti-apoptosis gene were down-regulated in HCT116-XIAP
−/−
cells. Relative to HCT116-XIAP
+/+
cells treated with troglitazone, 137 genes were up-regulated, and 31 genes were down-regulated in troglitazone-treated HCT116-XIAP
−/−
cells, all by ≥4-fold. Among the up-regulated genes were two anti-angiogenesis genes, seven pro-apoptosis genes, and six anti-proliferation genes. Among the down-regulated genes were one anti-angiogenesis gene, one pro-angiogenesis gene, one anti-apoptosis gene, one anti-proliferation gene, and two pro-proliferation genes.
Conclusion
Down-regulation of XIAP in HCT116 cells with or without troglitazone treatment was associated with changes of gene expression that favor increased tendency of apoptosis, decreased cell proliferation, and angiogenesis potential.</description><identifier>ISSN: 0179-1958</identifier><identifier>EISSN: 1432-1262</identifier><identifier>DOI: 10.1007/s00384-008-0566-1</identifier><identifier>PMID: 18704457</identifier><identifier>CODEN: IJCDE6</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer-Verlag</publisher><subject>Apoptosis - drug effects ; Apoptosis - genetics ; Biological and medical sciences ; Blotting, Western ; Cell Proliferation - drug effects ; Chromans - pharmacology ; Colonic Neoplasms - genetics ; Colonic Neoplasms - pathology ; Gastroenterology ; Gastroenterology. Liver. Pancreas. Abdomen ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic - drug effects ; HCT116 Cells ; Hepatology ; Humans ; Internal Medicine ; Medical sciences ; Medicine ; Medicine & Public Health ; Neovascularization, Pathologic - genetics ; Oligonucleotide Array Sequence Analysis ; Original Article ; Proctology ; Reproducibility of Results ; Reverse Transcriptase Polymerase Chain Reaction ; Stomach. Duodenum. Small intestine. Colon. Rectum. Anus ; Surgery ; Thiazolidinediones - pharmacology ; Tumors ; X-Linked Inhibitor of Apoptosis Protein - genetics ; X-Linked Inhibitor of Apoptosis Protein - metabolism</subject><ispartof>International journal of colorectal disease, 2009-03, Vol.24 (3), p.245-260</ispartof><rights>Springer-Verlag 2008</rights><rights>2009 INIST-CNRS</rights><rights>Springer-Verlag 2009</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c430t-5742750ad47b3e2e8f96bfdffefc3a05ca81ef93776fde45ea5abc10f15c127a3</citedby><cites>FETCH-LOGICAL-c430t-5742750ad47b3e2e8f96bfdffefc3a05ca81ef93776fde45ea5abc10f15c127a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00384-008-0566-1$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00384-008-0566-1$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=21071454$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18704457$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Qiao, Liang</creatorcontrib><creatorcontrib>Li, Gloria H. Y.</creatorcontrib><creatorcontrib>Dai, Yun</creatorcontrib><creatorcontrib>Wang, Jide</creatorcontrib><creatorcontrib>Li, Zesong</creatorcontrib><creatorcontrib>Zou, Bing</creatorcontrib><creatorcontrib>Gu, Qing</creatorcontrib><creatorcontrib>Ma, Juan</creatorcontrib><creatorcontrib>Pang, R.</creatorcontrib><creatorcontrib>Lan, Hui Y.</creatorcontrib><creatorcontrib>Wong, Benjamin C. Y.</creatorcontrib><title>Gene expression profile in colon cancer cells with respect to XIAP expression status</title><title>International journal of colorectal disease</title><addtitle>Int J Colorectal Dis</addtitle><addtitle>Int J Colorectal Dis</addtitle><description>Background and aims
We observed a marked synergism between peroxisome proliferator-activated receptor gamma (PPARγ) ligands and X-linked inhibitor of apoptosis (XIAP) down-regulation in colon cancer. In the current study, we detected the gene expression profile in HCT116 cells treated with or without PPARγ ligand troglitazone.
Materials and methods
HCT116-XIAP
+/+
and HCT116-XIAP
−/−
cells were treated with or without 50 μM troglitazone for 48 h. Gene expressions were detected by microarray, and selected genes were validated by reverse-transcriptase polymerase chain reaction (PCR), real-time PCR, and Western blot.
Results
Relative to HCT116-XIAP
+/+
cells, 58 genes were up-regulated and 33 genes down-regulated in HCT116-XIAP
−/−
cells, all by ≥4-fold. These genes could be classified into a wide variety of functional classes, but we focused on those related to angiogenesis, apoptosis, and proliferation. Thus, two pro-apoptotic genes and one pro-proliferation gene were up-regulated in HCT116-XIAP
−/−
cells. Two pro-proliferation genes, one pro-angiogenesis gene, one anti-angiogenesis gene, and one anti-apoptosis gene were down-regulated in HCT116-XIAP
−/−
cells. Relative to HCT116-XIAP
+/+
cells treated with troglitazone, 137 genes were up-regulated, and 31 genes were down-regulated in troglitazone-treated HCT116-XIAP
−/−
cells, all by ≥4-fold. Among the up-regulated genes were two anti-angiogenesis genes, seven pro-apoptosis genes, and six anti-proliferation genes. Among the down-regulated genes were one anti-angiogenesis gene, one pro-angiogenesis gene, one anti-apoptosis gene, one anti-proliferation gene, and two pro-proliferation genes.
Conclusion
Down-regulation of XIAP in HCT116 cells with or without troglitazone treatment was associated with changes of gene expression that favor increased tendency of apoptosis, decreased cell proliferation, and angiogenesis potential.</description><subject>Apoptosis - drug effects</subject><subject>Apoptosis - genetics</subject><subject>Biological and medical sciences</subject><subject>Blotting, Western</subject><subject>Cell Proliferation - drug effects</subject><subject>Chromans - pharmacology</subject><subject>Colonic Neoplasms - genetics</subject><subject>Colonic Neoplasms - pathology</subject><subject>Gastroenterology</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Gene Expression Profiling</subject><subject>Gene Expression Regulation, Neoplastic - drug effects</subject><subject>HCT116 Cells</subject><subject>Hepatology</subject><subject>Humans</subject><subject>Internal Medicine</subject><subject>Medical sciences</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Neovascularization, Pathologic - genetics</subject><subject>Oligonucleotide Array Sequence Analysis</subject><subject>Original Article</subject><subject>Proctology</subject><subject>Reproducibility of Results</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</subject><subject>Surgery</subject><subject>Thiazolidinediones - pharmacology</subject><subject>Tumors</subject><subject>X-Linked Inhibitor of Apoptosis Protein - genetics</subject><subject>X-Linked Inhibitor of Apoptosis Protein - metabolism</subject><issn>0179-1958</issn><issn>1432-1262</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNp1kMFqGzEQhkVJaJy0D9BLEYHmts2MVlqtj8GkTsCQHBLoTcjyqN2w3nU1uyR5-8rY1KGQk5D0_TM_nxBfEL4jgL1kgLLWBUBdgKmqAj-ICepSFagqdSQmgHZa4NTUJ-KU-QnyvbL6ozjB2oLWxk7Ew5w6kvSyScTc9J3cpD42Lcmmk6Fv80PwXaAkA7Uty-dm-C0zuqEwyKGXP2-v7t-mefDDyJ_EcfQt0-f9eSYef1w_zG6Kxd38dna1KIIuYSiM1coa8CttlyUpquO0WsZVjBRD6cEEXyPFaWltFVekDXnjlwEhogmorC_PxMVubi79ZyQe3LrhbVHfUT-yU6Ch1JXK4Pl_4FM_pi53cworo9BAnSHcQSH1zImi26Rm7dOrQ3Bb327n22XfbuvbYc583Q8el2taHRJ7wRn4tgc8B9_GlG02_I9TCBa10ZlTO47zV_eL0qHh-9v_AqXdmB8</recordid><startdate>20090301</startdate><enddate>20090301</enddate><creator>Qiao, Liang</creator><creator>Li, Gloria H. Y.</creator><creator>Dai, Yun</creator><creator>Wang, Jide</creator><creator>Li, Zesong</creator><creator>Zou, Bing</creator><creator>Gu, Qing</creator><creator>Ma, Juan</creator><creator>Pang, R.</creator><creator>Lan, Hui Y.</creator><creator>Wong, Benjamin C. Y.</creator><general>Springer-Verlag</general><general>Springer</general><general>Springer Nature B.V</general><scope>IQODW</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>3V.</scope><scope>7T5</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7QO</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope></search><sort><creationdate>20090301</creationdate><title>Gene expression profile in colon cancer cells with respect to XIAP expression status</title><author>Qiao, Liang ; Li, Gloria H. Y. ; Dai, Yun ; Wang, Jide ; Li, Zesong ; Zou, Bing ; Gu, Qing ; Ma, Juan ; Pang, R. ; Lan, Hui Y. ; Wong, Benjamin C. Y.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c430t-5742750ad47b3e2e8f96bfdffefc3a05ca81ef93776fde45ea5abc10f15c127a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Apoptosis - drug effects</topic><topic>Apoptosis - genetics</topic><topic>Biological and medical sciences</topic><topic>Blotting, Western</topic><topic>Cell Proliferation - drug effects</topic><topic>Chromans - pharmacology</topic><topic>Colonic Neoplasms - genetics</topic><topic>Colonic Neoplasms - pathology</topic><topic>Gastroenterology</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Gene Expression Profiling</topic><topic>Gene Expression Regulation, Neoplastic - drug effects</topic><topic>HCT116 Cells</topic><topic>Hepatology</topic><topic>Humans</topic><topic>Internal Medicine</topic><topic>Medical sciences</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Neovascularization, Pathologic - genetics</topic><topic>Oligonucleotide Array Sequence Analysis</topic><topic>Original Article</topic><topic>Proctology</topic><topic>Reproducibility of Results</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</topic><topic>Surgery</topic><topic>Thiazolidinediones - pharmacology</topic><topic>Tumors</topic><topic>X-Linked Inhibitor of Apoptosis Protein - genetics</topic><topic>X-Linked Inhibitor of Apoptosis Protein - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Qiao, Liang</creatorcontrib><creatorcontrib>Li, Gloria H. Y.</creatorcontrib><creatorcontrib>Dai, Yun</creatorcontrib><creatorcontrib>Wang, Jide</creatorcontrib><creatorcontrib>Li, Zesong</creatorcontrib><creatorcontrib>Zou, Bing</creatorcontrib><creatorcontrib>Gu, Qing</creatorcontrib><creatorcontrib>Ma, Juan</creatorcontrib><creatorcontrib>Pang, R.</creatorcontrib><creatorcontrib>Lan, Hui Y.</creatorcontrib><creatorcontrib>Wong, Benjamin C. Y.</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Biotechnology Research Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><jtitle>International journal of colorectal disease</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Qiao, Liang</au><au>Li, Gloria H. Y.</au><au>Dai, Yun</au><au>Wang, Jide</au><au>Li, Zesong</au><au>Zou, Bing</au><au>Gu, Qing</au><au>Ma, Juan</au><au>Pang, R.</au><au>Lan, Hui Y.</au><au>Wong, Benjamin C. Y.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Gene expression profile in colon cancer cells with respect to XIAP expression status</atitle><jtitle>International journal of colorectal disease</jtitle><stitle>Int J Colorectal Dis</stitle><addtitle>Int J Colorectal Dis</addtitle><date>2009-03-01</date><risdate>2009</risdate><volume>24</volume><issue>3</issue><spage>245</spage><epage>260</epage><pages>245-260</pages><issn>0179-1958</issn><eissn>1432-1262</eissn><coden>IJCDE6</coden><abstract>Background and aims
We observed a marked synergism between peroxisome proliferator-activated receptor gamma (PPARγ) ligands and X-linked inhibitor of apoptosis (XIAP) down-regulation in colon cancer. In the current study, we detected the gene expression profile in HCT116 cells treated with or without PPARγ ligand troglitazone.
Materials and methods
HCT116-XIAP
+/+
and HCT116-XIAP
−/−
cells were treated with or without 50 μM troglitazone for 48 h. Gene expressions were detected by microarray, and selected genes were validated by reverse-transcriptase polymerase chain reaction (PCR), real-time PCR, and Western blot.
Results
Relative to HCT116-XIAP
+/+
cells, 58 genes were up-regulated and 33 genes down-regulated in HCT116-XIAP
−/−
cells, all by ≥4-fold. These genes could be classified into a wide variety of functional classes, but we focused on those related to angiogenesis, apoptosis, and proliferation. Thus, two pro-apoptotic genes and one pro-proliferation gene were up-regulated in HCT116-XIAP
−/−
cells. Two pro-proliferation genes, one pro-angiogenesis gene, one anti-angiogenesis gene, and one anti-apoptosis gene were down-regulated in HCT116-XIAP
−/−
cells. Relative to HCT116-XIAP
+/+
cells treated with troglitazone, 137 genes were up-regulated, and 31 genes were down-regulated in troglitazone-treated HCT116-XIAP
−/−
cells, all by ≥4-fold. Among the up-regulated genes were two anti-angiogenesis genes, seven pro-apoptosis genes, and six anti-proliferation genes. Among the down-regulated genes were one anti-angiogenesis gene, one pro-angiogenesis gene, one anti-apoptosis gene, one anti-proliferation gene, and two pro-proliferation genes.
Conclusion
Down-regulation of XIAP in HCT116 cells with or without troglitazone treatment was associated with changes of gene expression that favor increased tendency of apoptosis, decreased cell proliferation, and angiogenesis potential.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer-Verlag</pub><pmid>18704457</pmid><doi>10.1007/s00384-008-0566-1</doi><tpages>16</tpages></addata></record> |
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language | eng |
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subjects | Apoptosis - drug effects Apoptosis - genetics Biological and medical sciences Blotting, Western Cell Proliferation - drug effects Chromans - pharmacology Colonic Neoplasms - genetics Colonic Neoplasms - pathology Gastroenterology Gastroenterology. Liver. Pancreas. Abdomen Gene Expression Profiling Gene Expression Regulation, Neoplastic - drug effects HCT116 Cells Hepatology Humans Internal Medicine Medical sciences Medicine Medicine & Public Health Neovascularization, Pathologic - genetics Oligonucleotide Array Sequence Analysis Original Article Proctology Reproducibility of Results Reverse Transcriptase Polymerase Chain Reaction Stomach. Duodenum. Small intestine. Colon. Rectum. Anus Surgery Thiazolidinediones - pharmacology Tumors X-Linked Inhibitor of Apoptosis Protein - genetics X-Linked Inhibitor of Apoptosis Protein - metabolism |
title | Gene expression profile in colon cancer cells with respect to XIAP expression status |
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