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
Hauptverfasser: 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.
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container_end_page 260
container_issue 3
container_start_page 245
container_title International journal of colorectal disease
container_volume 24
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
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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 &amp; 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&amp;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 &amp; 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. 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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 &amp; 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. 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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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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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