Microarray-based detection and expression analysis of extracellular matrix proteins in drug-resistant ovarian cancer cell lines
Ovarian cancer is the most lethal gynecological malignancy. Multiple drug resistance (MDR) development leads to resistance of cancer cells to chemotherapy. Microarray methods can provide information regarding new candidate genes that can play a role in resistance to cytostatic drugs. Extracellular m...
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| Veröffentlicht in: | Oncology reports 2014-11, Vol.32 (5), p.1981-1990 |
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| container_issue | 5 |
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| container_title | Oncology reports |
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| creator | JANUCHOWSKI, RADOSŁAW ZAWIERUCHA, PIOTR RUCIŃSKI, MARCIN ZABEL, MACIEJ |
| description | Ovarian cancer is the most lethal gynecological malignancy. Multiple drug resistance (MDR) development leads to resistance of cancer cells to chemotherapy. Microarray methods can provide information regarding new candidate genes that can play a role in resistance to cytostatic drugs. Extracellular matrix (ECM) can influence drug resistance by inhibiting the penetration of the drug into cancer tissue as well as increased apoptosis resistance. In the present study, we report changes in the ECM and related gene expression pattern in methotrexate-, cisplatin-, doxorubicin-, vincristine-, topotecan- and paclitaxel-resistant variants of the W1 ovarian cancer cell line. The resistant variants of the W1 cell line were generated by stepwise selection of cells with an increasing concentration of the indicated drugs. Affymetrix GeneChip® Human Genome U219 Array Strips were used for hybridizations. Independent t-tests were used to determinate the statistical significance of results. Genes whose expression levels were higher than the assumed threshold (upregulated, >5-fold and downregulated, 20-fold. These genes were: ITGB1BP3, COL3A1, COL5A2, COL15A1, TGFBI, DCN, LUM, MATN2, POSTN and EGFL6. The expression of seven genes decreased very significantly: ITGA1, COL1A2, LAMA2, GPC3, KRT23, VIT and HMCN1. The expression pattern of ECM and related genes provided the preliminary view into the role of ECM components in cytostatic drug resistance of cancer cells. The exact role of the investigated genes in drug resistance requires further investigation. |
| doi_str_mv | 10.3892/or.2014.3468 |
| format | Article |
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Multiple drug resistance (MDR) development leads to resistance of cancer cells to chemotherapy. Microarray methods can provide information regarding new candidate genes that can play a role in resistance to cytostatic drugs. Extracellular matrix (ECM) can influence drug resistance by inhibiting the penetration of the drug into cancer tissue as well as increased apoptosis resistance. In the present study, we report changes in the ECM and related gene expression pattern in methotrexate-, cisplatin-, doxorubicin-, vincristine-, topotecan- and paclitaxel-resistant variants of the W1 ovarian cancer cell line. The resistant variants of the W1 cell line were generated by stepwise selection of cells with an increasing concentration of the indicated drugs. Affymetrix GeneChip® Human Genome U219 Array Strips were used for hybridizations. Independent t-tests were used to determinate the statistical significance of results. Genes whose expression levels were higher than the assumed threshold (upregulated, >5-fold and downregulated, <5-fold) were visualized using the scatter plot method, selected and listed in the tables. Among the investigated genes, expression of 24 genes increased, expression of 14 genes decreased and expression of three genes increased or decreased depending on the cell line. Among the increased genes, expression of 10 increased very significantly, >20-fold. These genes were: ITGB1BP3, COL3A1, COL5A2, COL15A1, TGFBI, DCN, LUM, MATN2, POSTN and EGFL6. The expression of seven genes decreased very significantly: ITGA1, COL1A2, LAMA2, GPC3, KRT23, VIT and HMCN1. The expression pattern of ECM and related genes provided the preliminary view into the role of ECM components in cytostatic drug resistance of cancer cells. The exact role of the investigated genes in drug resistance requires further investigation.</description><identifier>ISSN: 1021-335X</identifier><identifier>EISSN: 1791-2431</identifier><identifier>DOI: 10.3892/or.2014.3468</identifier><identifier>PMID: 25199881</identifier><language>eng</language><publisher>Greece: D.A. Spandidos</publisher><subject>Antineoplastic Agents - pharmacology ; Apoptosis ; Cancer ; Cancer therapies ; cDNA microarray ; Cell growth ; Cell Line, Tumor ; Chemotherapy ; Drug resistance ; Drug Resistance, Neoplasm ; Extracellular matrix ; Extracellular Matrix Proteins - genetics ; Female ; Gene expression ; Gene Expression Profiling - methods ; Gene Expression Regulation, Neoplastic ; Genetic aspects ; Genomes ; Humans ; Metastasis ; multidrug resistance ; Oligonucleotide Array Sequence Analysis - methods ; Oncology, Experimental ; Ovarian cancer ; Ovarian Neoplasms - drug therapy ; Ovarian Neoplasms - genetics ; Penicillin ; Physiological aspects ; Proteins</subject><ispartof>Oncology reports, 2014-11, Vol.32 (5), p.1981-1990</ispartof><rights>Copyright © 2014, Spandidos Publications</rights><rights>COPYRIGHT 2014 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2014</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c416t-46e927de21503d2dccf429d1e4ab1fedf25ebb7b45884ccfeac3bf8438cef0e83</citedby><cites>FETCH-LOGICAL-c416t-46e927de21503d2dccf429d1e4ab1fedf25ebb7b45884ccfeac3bf8438cef0e83</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27923,27924</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25199881$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>JANUCHOWSKI, RADOSŁAW</creatorcontrib><creatorcontrib>ZAWIERUCHA, PIOTR</creatorcontrib><creatorcontrib>RUCIŃSKI, MARCIN</creatorcontrib><creatorcontrib>ZABEL, MACIEJ</creatorcontrib><title>Microarray-based detection and expression analysis of extracellular matrix proteins in drug-resistant ovarian cancer cell lines</title><title>Oncology reports</title><addtitle>Oncol Rep</addtitle><description>Ovarian cancer is the most lethal gynecological malignancy. Multiple drug resistance (MDR) development leads to resistance of cancer cells to chemotherapy. Microarray methods can provide information regarding new candidate genes that can play a role in resistance to cytostatic drugs. Extracellular matrix (ECM) can influence drug resistance by inhibiting the penetration of the drug into cancer tissue as well as increased apoptosis resistance. In the present study, we report changes in the ECM and related gene expression pattern in methotrexate-, cisplatin-, doxorubicin-, vincristine-, topotecan- and paclitaxel-resistant variants of the W1 ovarian cancer cell line. The resistant variants of the W1 cell line were generated by stepwise selection of cells with an increasing concentration of the indicated drugs. Affymetrix GeneChip® Human Genome U219 Array Strips were used for hybridizations. Independent t-tests were used to determinate the statistical significance of results. Genes whose expression levels were higher than the assumed threshold (upregulated, >5-fold and downregulated, <5-fold) were visualized using the scatter plot method, selected and listed in the tables. Among the investigated genes, expression of 24 genes increased, expression of 14 genes decreased and expression of three genes increased or decreased depending on the cell line. Among the increased genes, expression of 10 increased very significantly, >20-fold. These genes were: ITGB1BP3, COL3A1, COL5A2, COL15A1, TGFBI, DCN, LUM, MATN2, POSTN and EGFL6. The expression of seven genes decreased very significantly: ITGA1, COL1A2, LAMA2, GPC3, KRT23, VIT and HMCN1. The expression pattern of ECM and related genes provided the preliminary view into the role of ECM components in cytostatic drug resistance of cancer cells. The exact role of the investigated genes in drug resistance requires further investigation.</description><subject>Antineoplastic Agents - pharmacology</subject><subject>Apoptosis</subject><subject>Cancer</subject><subject>Cancer therapies</subject><subject>cDNA microarray</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Chemotherapy</subject><subject>Drug resistance</subject><subject>Drug Resistance, Neoplasm</subject><subject>Extracellular matrix</subject><subject>Extracellular Matrix Proteins - genetics</subject><subject>Female</subject><subject>Gene expression</subject><subject>Gene Expression Profiling - methods</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Genetic aspects</subject><subject>Genomes</subject><subject>Humans</subject><subject>Metastasis</subject><subject>multidrug resistance</subject><subject>Oligonucleotide Array Sequence Analysis - methods</subject><subject>Oncology, Experimental</subject><subject>Ovarian cancer</subject><subject>Ovarian Neoplasms - drug therapy</subject><subject>Ovarian Neoplasms - genetics</subject><subject>Penicillin</subject><subject>Physiological aspects</subject><subject>Proteins</subject><issn>1021-335X</issn><issn>1791-2431</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNptkk1vFSEUhidGY2t159qQmJgu5MrXzMCyaaya1LjRxB1h4NDSzMAVZprelX9dJrderTEsgMPzHs5X07ykZMOlYu9S3jBCxYaLTj5qjmmvKGaC08f1TBjFnLffj5pnpdwQwnrSqafNEWupUlLS4-bn52BzMjmbHR5MAYcczGDnkCIy0SG422YoZX81466EgpKv5jkbC-O4jCajycw53KFtTjOEWFCIyOXlCldlKLOJM0q3JgcTkTXRQkarEo0hQnnePPFmLPDifj9pvl28_3r-EV9--fDp_OwSW0G7GYsOFOsdMNoS7piz1gumHAVhBurBedbCMPSDaKUU9RGM5YOXgksLnoDkJ83p3m8N8scCZdZTKGsYJkJaiqYd5Uowolb09T_oTVpyTb5SirOul7zCB-rKjKBD9GmtyOpUn1VPtbyEsUpt_kPV5WAKNkXwodofCN78JbgGM87XJY3L2pDyEHy7B2v7Ssng9TaHyeSdpkSvg6FT1utg6HUwKv7qPqllmMAd4N-T8Ofjsq19Dy6VA5My5gyTFlNVwV_q4cGA</recordid><startdate>20141101</startdate><enddate>20141101</enddate><creator>JANUCHOWSKI, RADOSŁAW</creator><creator>ZAWIERUCHA, PIOTR</creator><creator>RUCIŃSKI, MARCIN</creator><creator>ZABEL, MACIEJ</creator><general>D.A. Spandidos</general><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</general><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>7X7</scope><scope>7XB</scope><scope>88E</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>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20141101</creationdate><title>Microarray-based detection and expression analysis of extracellular matrix proteins in drug-resistant ovarian cancer cell lines</title><author>JANUCHOWSKI, RADOSŁAW ; ZAWIERUCHA, PIOTR ; RUCIŃSKI, MARCIN ; ZABEL, MACIEJ</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c416t-46e927de21503d2dccf429d1e4ab1fedf25ebb7b45884ccfeac3bf8438cef0e83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Antineoplastic Agents - pharmacology</topic><topic>Apoptosis</topic><topic>Cancer</topic><topic>Cancer therapies</topic><topic>cDNA microarray</topic><topic>Cell growth</topic><topic>Cell Line, Tumor</topic><topic>Chemotherapy</topic><topic>Drug resistance</topic><topic>Drug Resistance, Neoplasm</topic><topic>Extracellular matrix</topic><topic>Extracellular Matrix Proteins - genetics</topic><topic>Female</topic><topic>Gene expression</topic><topic>Gene Expression Profiling - methods</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Genetic aspects</topic><topic>Genomes</topic><topic>Humans</topic><topic>Metastasis</topic><topic>multidrug resistance</topic><topic>Oligonucleotide Array Sequence Analysis - methods</topic><topic>Oncology, Experimental</topic><topic>Ovarian cancer</topic><topic>Ovarian Neoplasms - drug therapy</topic><topic>Ovarian Neoplasms - genetics</topic><topic>Penicillin</topic><topic>Physiological aspects</topic><topic>Proteins</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>JANUCHOWSKI, RADOSŁAW</creatorcontrib><creatorcontrib>ZAWIERUCHA, PIOTR</creatorcontrib><creatorcontrib>RUCIŃSKI, MARCIN</creatorcontrib><creatorcontrib>ZABEL, MACIEJ</creatorcontrib><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>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</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>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>MEDLINE - Academic</collection><jtitle>Oncology reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>JANUCHOWSKI, RADOSŁAW</au><au>ZAWIERUCHA, PIOTR</au><au>RUCIŃSKI, MARCIN</au><au>ZABEL, MACIEJ</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Microarray-based detection and expression analysis of extracellular matrix proteins in drug-resistant ovarian cancer cell lines</atitle><jtitle>Oncology reports</jtitle><addtitle>Oncol Rep</addtitle><date>2014-11-01</date><risdate>2014</risdate><volume>32</volume><issue>5</issue><spage>1981</spage><epage>1990</epage><pages>1981-1990</pages><issn>1021-335X</issn><eissn>1791-2431</eissn><abstract>Ovarian cancer is the most lethal gynecological malignancy. Multiple drug resistance (MDR) development leads to resistance of cancer cells to chemotherapy. Microarray methods can provide information regarding new candidate genes that can play a role in resistance to cytostatic drugs. Extracellular matrix (ECM) can influence drug resistance by inhibiting the penetration of the drug into cancer tissue as well as increased apoptosis resistance. In the present study, we report changes in the ECM and related gene expression pattern in methotrexate-, cisplatin-, doxorubicin-, vincristine-, topotecan- and paclitaxel-resistant variants of the W1 ovarian cancer cell line. The resistant variants of the W1 cell line were generated by stepwise selection of cells with an increasing concentration of the indicated drugs. Affymetrix GeneChip® Human Genome U219 Array Strips were used for hybridizations. Independent t-tests were used to determinate the statistical significance of results. Genes whose expression levels were higher than the assumed threshold (upregulated, >5-fold and downregulated, <5-fold) were visualized using the scatter plot method, selected and listed in the tables. Among the investigated genes, expression of 24 genes increased, expression of 14 genes decreased and expression of three genes increased or decreased depending on the cell line. Among the increased genes, expression of 10 increased very significantly, >20-fold. These genes were: ITGB1BP3, COL3A1, COL5A2, COL15A1, TGFBI, DCN, LUM, MATN2, POSTN and EGFL6. The expression of seven genes decreased very significantly: ITGA1, COL1A2, LAMA2, GPC3, KRT23, VIT and HMCN1. The expression pattern of ECM and related genes provided the preliminary view into the role of ECM components in cytostatic drug resistance of cancer cells. The exact role of the investigated genes in drug resistance requires further investigation.</abstract><cop>Greece</cop><pub>D.A. Spandidos</pub><pmid>25199881</pmid><doi>10.3892/or.2014.3468</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Antineoplastic Agents - pharmacology Apoptosis Cancer Cancer therapies cDNA microarray Cell growth Cell Line, Tumor Chemotherapy Drug resistance Drug Resistance, Neoplasm Extracellular matrix Extracellular Matrix Proteins - genetics Female Gene expression Gene Expression Profiling - methods Gene Expression Regulation, Neoplastic Genetic aspects Genomes Humans Metastasis multidrug resistance Oligonucleotide Array Sequence Analysis - methods Oncology, Experimental Ovarian cancer Ovarian Neoplasms - drug therapy Ovarian Neoplasms - genetics Penicillin Physiological aspects Proteins |
| title | Microarray-based detection and expression analysis of extracellular matrix proteins in drug-resistant ovarian cancer cell lines |
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