Gene expression profile comparison between colorectal cancer and adjacent normal tissues
The present study aimed to compare gene expression profiles between colorectal cancer and adjacent normal tissues, and to perform a preliminarily analysis of the key genes and underlying molecular mechanisms implicated in colorectal cancer development. Gene expression microarray chips were used to s...
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Veröffentlicht in: | Oncology letters 2017-11, Vol.14 (5), p.6071-6078 |
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description | The present study aimed to compare gene expression profiles between colorectal cancer and adjacent normal tissues, and to perform a preliminarily analysis of the key genes and underlying molecular mechanisms implicated in colorectal cancer development. Gene expression microarray chips were used to screen genes that were differently expressed between colorectal cancer and adjacent normal tissues. Approximately 1,183 genes were differentially expressed in cancer tissues compared with adjacent normal tissues (P≤0.05; fold difference, >2.0), of which 570 genes were upregulated and 613 genes were downregulated. In total, 6 upregulated genes, including keratin 23, collagen type X α1, collagen type XI α1, cell migration-inducing hyaluronan-binding protein, transforming growth factor-β1 and V-Myc avian myelocytomatosis viral oncogene homolog, and 2 downregulated genes, including channel α subunit 7 and EPH receptor A7, were selected and validated using reverse transcription-quantitative polymerase chain reaction, which exhibited results that were consistent with the microarray analysis. These 1,183 differentially expressed genes were further classified into 71 groups based on their functions using gene ontology and pathway analyses. Kyoto Encyclopedia of Genes and Genomes analysis of these upregulated or downregulated genes suggested that 23 signaling pathways were involved. The present study preliminarily screened for and identified key genes and signaling pathways that may be closely associated with colorectal cancer development. However, subsequent gene function studies are required to verify these findings. |
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Gene expression microarray chips were used to screen genes that were differently expressed between colorectal cancer and adjacent normal tissues. Approximately 1,183 genes were differentially expressed in cancer tissues compared with adjacent normal tissues (P≤0.05; fold difference, >2.0), of which 570 genes were upregulated and 613 genes were downregulated. In total, 6 upregulated genes, including keratin 23, collagen type X α1, collagen type XI α1, cell migration-inducing hyaluronan-binding protein, transforming growth factor-β1 and V-Myc avian myelocytomatosis viral oncogene homolog, and 2 downregulated genes, including channel α subunit 7 and EPH receptor A7, were selected and validated using reverse transcription-quantitative polymerase chain reaction, which exhibited results that were consistent with the microarray analysis. These 1,183 differentially expressed genes were further classified into 71 groups based on their functions using gene ontology and pathway analyses. Kyoto Encyclopedia of Genes and Genomes analysis of these upregulated or downregulated genes suggested that 23 signaling pathways were involved. The present study preliminarily screened for and identified key genes and signaling pathways that may be closely associated with colorectal cancer development. However, subsequent gene function studies are required to verify these findings.</description><identifier>ISSN: 1792-1074</identifier><identifier>EISSN: 1792-1082</identifier><identifier>DOI: 10.3892/ol.2017.6915</identifier><identifier>PMID: 29113248</identifier><language>eng</language><publisher>Greece: D.A. Spandidos</publisher><subject>Care and treatment ; Cell adhesion & migration ; Cell cycle ; Collagen ; Colorectal cancer ; complementary DNA ; Development and progression ; Gene expression ; gene oncology analysis ; Genetic aspects ; Growth factors ; Health aspects ; Hybridization ; Keratin ; Medical screening ; microarray ; Oncogenes ; pathway analysis ; Polymerase chain reaction ; Proteins ; Software ; Studies</subject><ispartof>Oncology letters, 2017-11, Vol.14 (5), p.6071-6078</ispartof><rights>Copyright © 2017, Spandidos Publications</rights><rights>COPYRIGHT 2017 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2017</rights><rights>Copyright © 2017, Spandidos Publications 2017</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c539t-6280d405d36c5d1bf1c1548ded84744594f8663ad80ed89155df1da0389e5b8f3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5661416/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5661416/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,5556,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29113248$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yang, Qian</creatorcontrib><creatorcontrib>Feng, Maohui</creatorcontrib><creatorcontrib>Ma, Xiang</creatorcontrib><creatorcontrib>Li, Huachi</creatorcontrib><creatorcontrib>Xie, Wei</creatorcontrib><title>Gene expression profile comparison between colorectal cancer and adjacent normal tissues</title><title>Oncology letters</title><addtitle>Oncol Lett</addtitle><description>The present study aimed to compare gene expression profiles between colorectal cancer and adjacent normal tissues, and to perform a preliminarily analysis of the key genes and underlying molecular mechanisms implicated in colorectal cancer development. Gene expression microarray chips were used to screen genes that were differently expressed between colorectal cancer and adjacent normal tissues. Approximately 1,183 genes were differentially expressed in cancer tissues compared with adjacent normal tissues (P≤0.05; fold difference, >2.0), of which 570 genes were upregulated and 613 genes were downregulated. In total, 6 upregulated genes, including keratin 23, collagen type X α1, collagen type XI α1, cell migration-inducing hyaluronan-binding protein, transforming growth factor-β1 and V-Myc avian myelocytomatosis viral oncogene homolog, and 2 downregulated genes, including channel α subunit 7 and EPH receptor A7, were selected and validated using reverse transcription-quantitative polymerase chain reaction, which exhibited results that were consistent with the microarray analysis. These 1,183 differentially expressed genes were further classified into 71 groups based on their functions using gene ontology and pathway analyses. Kyoto Encyclopedia of Genes and Genomes analysis of these upregulated or downregulated genes suggested that 23 signaling pathways were involved. The present study preliminarily screened for and identified key genes and signaling pathways that may be closely associated with colorectal cancer development. However, subsequent gene function studies are required to verify these findings.</description><subject>Care and treatment</subject><subject>Cell adhesion & migration</subject><subject>Cell cycle</subject><subject>Collagen</subject><subject>Colorectal cancer</subject><subject>complementary DNA</subject><subject>Development and progression</subject><subject>Gene expression</subject><subject>gene oncology analysis</subject><subject>Genetic aspects</subject><subject>Growth factors</subject><subject>Health aspects</subject><subject>Hybridization</subject><subject>Keratin</subject><subject>Medical screening</subject><subject>microarray</subject><subject>Oncogenes</subject><subject>pathway analysis</subject><subject>Polymerase chain reaction</subject><subject>Proteins</subject><subject>Software</subject><subject>Studies</subject><issn>1792-1074</issn><issn>1792-1082</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>BENPR</sourceid><recordid>eNptks-L1DAUx4so7rLuzbMUFPFgxyZt0uSysCy6CgN7UfAWMsnrToY0qUnrj__eV2cdZsS8Q8J7n3yT96MonpN61QhJ30W_ojXpVlwS9qg4J52kFakFfXw4d-1ZcZnzrsbFOBGCPy3OqCSkoa04L77eQoASfo4JcnYxlGOKvfNQmjiMOrmMrg1MPwACunxMYCbtS6ODgVTqYEttd9pAmMoQ04ChyeU8Q35WPOm1z3D5sF8UXz68_3zzsVrf3X66uV5XhjVyqjgVtW1rZhtumCWbnhjCWmHBirZrWybbXnDeaCtqdGGWzPbE6hqzB7YRfXNRXO11x3kzgF1-krRXY3KDTr9U1E6dRoLbqvv4XTHOSUs4Crx5EEjxG358UoPLBrzXAeKcFZFYtVZ2UiL68h90F-cUMD2kBJMU9Y6oe-1BudBHfNcsouqa0UYSQbsOqdV_KDQLgzMxwNKF0wuvjy5sQftpm6OfJ-xaPgXf7kGTYs4J-kMxSK2WqVHRq2Vq1DI1iL84LuAB_jsjCLzaA3nEfjsb84G5W1c12h-d3xN1x8E</recordid><startdate>20171101</startdate><enddate>20171101</enddate><creator>Yang, Qian</creator><creator>Feng, Maohui</creator><creator>Ma, Xiang</creator><creator>Li, Huachi</creator><creator>Xie, Wei</creator><general>D.A. Spandidos</general><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20171101</creationdate><title>Gene expression profile comparison between colorectal cancer and adjacent normal tissues</title><author>Yang, Qian ; Feng, Maohui ; Ma, Xiang ; Li, Huachi ; Xie, Wei</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c539t-6280d405d36c5d1bf1c1548ded84744594f8663ad80ed89155df1da0389e5b8f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Care and treatment</topic><topic>Cell adhesion & migration</topic><topic>Cell cycle</topic><topic>Collagen</topic><topic>Colorectal cancer</topic><topic>complementary DNA</topic><topic>Development and progression</topic><topic>Gene expression</topic><topic>gene oncology analysis</topic><topic>Genetic aspects</topic><topic>Growth factors</topic><topic>Health aspects</topic><topic>Hybridization</topic><topic>Keratin</topic><topic>Medical screening</topic><topic>microarray</topic><topic>Oncogenes</topic><topic>pathway analysis</topic><topic>Polymerase chain reaction</topic><topic>Proteins</topic><topic>Software</topic><topic>Studies</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yang, Qian</creatorcontrib><creatorcontrib>Feng, Maohui</creatorcontrib><creatorcontrib>Ma, Xiang</creatorcontrib><creatorcontrib>Li, Huachi</creatorcontrib><creatorcontrib>Xie, Wei</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</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>British Nursing Database</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>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Oncology letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yang, Qian</au><au>Feng, Maohui</au><au>Ma, Xiang</au><au>Li, Huachi</au><au>Xie, Wei</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Gene expression profile comparison between colorectal cancer and adjacent normal tissues</atitle><jtitle>Oncology letters</jtitle><addtitle>Oncol Lett</addtitle><date>2017-11-01</date><risdate>2017</risdate><volume>14</volume><issue>5</issue><spage>6071</spage><epage>6078</epage><pages>6071-6078</pages><issn>1792-1074</issn><eissn>1792-1082</eissn><abstract>The present study aimed to compare gene expression profiles between colorectal cancer and adjacent normal tissues, and to perform a preliminarily analysis of the key genes and underlying molecular mechanisms implicated in colorectal cancer development. Gene expression microarray chips were used to screen genes that were differently expressed between colorectal cancer and adjacent normal tissues. Approximately 1,183 genes were differentially expressed in cancer tissues compared with adjacent normal tissues (P≤0.05; fold difference, >2.0), of which 570 genes were upregulated and 613 genes were downregulated. In total, 6 upregulated genes, including keratin 23, collagen type X α1, collagen type XI α1, cell migration-inducing hyaluronan-binding protein, transforming growth factor-β1 and V-Myc avian myelocytomatosis viral oncogene homolog, and 2 downregulated genes, including channel α subunit 7 and EPH receptor A7, were selected and validated using reverse transcription-quantitative polymerase chain reaction, which exhibited results that were consistent with the microarray analysis. These 1,183 differentially expressed genes were further classified into 71 groups based on their functions using gene ontology and pathway analyses. Kyoto Encyclopedia of Genes and Genomes analysis of these upregulated or downregulated genes suggested that 23 signaling pathways were involved. The present study preliminarily screened for and identified key genes and signaling pathways that may be closely associated with colorectal cancer development. However, subsequent gene function studies are required to verify these findings.</abstract><cop>Greece</cop><pub>D.A. Spandidos</pub><pmid>29113248</pmid><doi>10.3892/ol.2017.6915</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Care and treatment Cell adhesion & migration Cell cycle Collagen Colorectal cancer complementary DNA Development and progression Gene expression gene oncology analysis Genetic aspects Growth factors Health aspects Hybridization Keratin Medical screening microarray Oncogenes pathway analysis Polymerase chain reaction Proteins Software Studies |
title | Gene expression profile comparison between colorectal cancer and adjacent normal tissues |
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