The roles of FXYD family members in ovarian cancer: an integrated analysis by mining TCGA and GEO databases and functional validations
Background The FXYD family of ion transport regulators have emerged as important modulators of cancer progression and metastasis. However, their expression and roles in ovarian cancer (OCa) have not been systematically investigated. Methods The expression of FXYD genes in OCa was analyzed using data...
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| Veröffentlicht in: | Journal of cancer research and clinical oncology 2023-12, Vol.149 (19), p.17269-17284 |
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| creator | Zhao, Eryong Gao, Kefei Xiong, Jian Liu, Zhihong Chen, Yuelin Yi, Lisha |
| description | Background
The FXYD family of ion transport regulators have emerged as important modulators of cancer progression and metastasis. However, their expression and roles in ovarian cancer (OCa) have not been systematically investigated.
Methods
The expression of FXYD genes in OCa was analyzed using data from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO), as well as independent clinical samples. The prognostic values of FXYD genes were evaluated by Kaplan–Meier and Cox regression analysis. To explore potential mechanisms, bioinformatics approaches including Gene Ontology, KEGG pathway analysis, GSEA and drug sensitivity correlation analysis were performed. OCa cell lines overexpressing FXYD1, FXYD5 or FXYD7 were also generated and their impacts on proliferation, migration and invasion were assessed.
Results
FXYD1 and FXYD6 were significantly downregulated while FXYD3, FXYD4 and FXYD5 were upregulated in OCa tissues compared to normal tissues. FXYD1, FXYD5 and FXYD7 were independent adverse prognostic factors for OCa patients. Pathway and drug correlation analysis revealed that FXYD1, FXYD5 and FXYD7 genes regulated diverse oncogenic signaling cascades and modulated the response to various chemotherapeutic agents. Overexpression of FXYD1, FXYD5 or FXYD7 enhanced OCa cell motility and invasiveness in vitro.
Conclusion
Our results demonstrate aberrant expression patterns, prognostic values, and oncogenic activities of FXYD genes in OCa. FXYD1, FXYD5 and FXYD7 may serve as biomarkers and therapeutic targets for this disease. Targeting FXYD-mediated signaling represents a promising therapeutic strategy against OCa. |
| doi_str_mv | 10.1007/s00432-023-05445-z |
| format | Article |
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The FXYD family of ion transport regulators have emerged as important modulators of cancer progression and metastasis. However, their expression and roles in ovarian cancer (OCa) have not been systematically investigated.
Methods
The expression of FXYD genes in OCa was analyzed using data from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO), as well as independent clinical samples. The prognostic values of FXYD genes were evaluated by Kaplan–Meier and Cox regression analysis. To explore potential mechanisms, bioinformatics approaches including Gene Ontology, KEGG pathway analysis, GSEA and drug sensitivity correlation analysis were performed. OCa cell lines overexpressing FXYD1, FXYD5 or FXYD7 were also generated and their impacts on proliferation, migration and invasion were assessed.
Results
FXYD1 and FXYD6 were significantly downregulated while FXYD3, FXYD4 and FXYD5 were upregulated in OCa tissues compared to normal tissues. FXYD1, FXYD5 and FXYD7 were independent adverse prognostic factors for OCa patients. Pathway and drug correlation analysis revealed that FXYD1, FXYD5 and FXYD7 genes regulated diverse oncogenic signaling cascades and modulated the response to various chemotherapeutic agents. Overexpression of FXYD1, FXYD5 or FXYD7 enhanced OCa cell motility and invasiveness in vitro.
Conclusion
Our results demonstrate aberrant expression patterns, prognostic values, and oncogenic activities of FXYD genes in OCa. FXYD1, FXYD5 and FXYD7 may serve as biomarkers and therapeutic targets for this disease. Targeting FXYD-mediated signaling represents a promising therapeutic strategy against OCa.</description><identifier>ISSN: 0171-5216</identifier><identifier>EISSN: 1432-1335</identifier><identifier>DOI: 10.1007/s00432-023-05445-z</identifier><identifier>PMID: 37814066</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Bioinformatics ; biomarkers ; Cancer Research ; cell movement ; Cell Movement - genetics ; Chemotherapy ; Correlation analysis ; drug therapy ; drugs ; family ; Female ; Gene expression ; gene ontology ; Genes ; genome ; Genomes ; Hematology ; Humans ; Internal Medicine ; Invasiveness ; Ion Channels ; Medicine ; Medicine & Public Health ; Membrane Proteins - genetics ; Membrane Proteins - metabolism ; Metastases ; metastasis ; Microfilament Proteins - metabolism ; neoplasm progression ; Neoplasm Proteins - genetics ; Oncology ; Ovarian cancer ; ovarian neoplasms ; Ovarian Neoplasms - genetics ; regression analysis ; Signal transduction ; Sodium-Potassium-Exchanging ATPase - genetics ; Sodium-Potassium-Exchanging ATPase - metabolism ; Therapeutic targets</subject><ispartof>Journal of cancer research and clinical oncology, 2023-12, Vol.149 (19), p.17269-17284</ispartof><rights>The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.</rights><rights>2023. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c408t-38390bbb2ea98a1b3babf65cd2211cb64c130b29c12b49b9b9242c8a3de569f23</citedby><cites>FETCH-LOGICAL-c408t-38390bbb2ea98a1b3babf65cd2211cb64c130b29c12b49b9b9242c8a3de569f23</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/s00432-023-05445-z$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00432-023-05445-z$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/37814066$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhao, Eryong</creatorcontrib><creatorcontrib>Gao, Kefei</creatorcontrib><creatorcontrib>Xiong, Jian</creatorcontrib><creatorcontrib>Liu, Zhihong</creatorcontrib><creatorcontrib>Chen, Yuelin</creatorcontrib><creatorcontrib>Yi, Lisha</creatorcontrib><title>The roles of FXYD family members in ovarian cancer: an integrated analysis by mining TCGA and GEO databases and functional validations</title><title>Journal of cancer research and clinical oncology</title><addtitle>J Cancer Res Clin Oncol</addtitle><addtitle>J Cancer Res Clin Oncol</addtitle><description>Background
The FXYD family of ion transport regulators have emerged as important modulators of cancer progression and metastasis. However, their expression and roles in ovarian cancer (OCa) have not been systematically investigated.
Methods
The expression of FXYD genes in OCa was analyzed using data from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO), as well as independent clinical samples. The prognostic values of FXYD genes were evaluated by Kaplan–Meier and Cox regression analysis. To explore potential mechanisms, bioinformatics approaches including Gene Ontology, KEGG pathway analysis, GSEA and drug sensitivity correlation analysis were performed. OCa cell lines overexpressing FXYD1, FXYD5 or FXYD7 were also generated and their impacts on proliferation, migration and invasion were assessed.
Results
FXYD1 and FXYD6 were significantly downregulated while FXYD3, FXYD4 and FXYD5 were upregulated in OCa tissues compared to normal tissues. FXYD1, FXYD5 and FXYD7 were independent adverse prognostic factors for OCa patients. Pathway and drug correlation analysis revealed that FXYD1, FXYD5 and FXYD7 genes regulated diverse oncogenic signaling cascades and modulated the response to various chemotherapeutic agents. Overexpression of FXYD1, FXYD5 or FXYD7 enhanced OCa cell motility and invasiveness in vitro.
Conclusion
Our results demonstrate aberrant expression patterns, prognostic values, and oncogenic activities of FXYD genes in OCa. FXYD1, FXYD5 and FXYD7 may serve as biomarkers and therapeutic targets for this disease. Targeting FXYD-mediated signaling represents a promising therapeutic strategy against OCa.</description><subject>Bioinformatics</subject><subject>biomarkers</subject><subject>Cancer Research</subject><subject>cell movement</subject><subject>Cell Movement - genetics</subject><subject>Chemotherapy</subject><subject>Correlation analysis</subject><subject>drug therapy</subject><subject>drugs</subject><subject>family</subject><subject>Female</subject><subject>Gene expression</subject><subject>gene ontology</subject><subject>Genes</subject><subject>genome</subject><subject>Genomes</subject><subject>Hematology</subject><subject>Humans</subject><subject>Internal Medicine</subject><subject>Invasiveness</subject><subject>Ion Channels</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Membrane Proteins - genetics</subject><subject>Membrane Proteins - metabolism</subject><subject>Metastases</subject><subject>metastasis</subject><subject>Microfilament Proteins - metabolism</subject><subject>neoplasm progression</subject><subject>Neoplasm Proteins - genetics</subject><subject>Oncology</subject><subject>Ovarian cancer</subject><subject>ovarian neoplasms</subject><subject>Ovarian Neoplasms - genetics</subject><subject>regression analysis</subject><subject>Signal transduction</subject><subject>Sodium-Potassium-Exchanging ATPase - genetics</subject><subject>Sodium-Potassium-Exchanging ATPase - metabolism</subject><subject>Therapeutic targets</subject><issn>0171-5216</issn><issn>1432-1335</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqFkc1u1DAUhS0EotOBF2CBLLFhE_D1T37YVdN2QKrUzSDByrIdZ3CVOMVOKk0fgOfuHaZQqYtWXtj3-jvnyj6EvAP2CRirPmfGpOAF46JgSkpV3L4gC9i3QAj1kiwYVFAoDuUROc75imGtKv6aHImqBsnKckH-bH55msbeZzp29PzHz1PamSH0Ozr4wfqUaYh0vDEpmEidic6nLxSPIU5-m8zkW6xMv8shU4uiEEPc0s1qfYL9lq7PLmlrJmNNxgn7TjdHN4URNfTG9AEvschvyKvO9Nm_vd-X5Pv52Wb1tbi4XH9bnVwUTrJ6KkQtGmat5d40tQErrLFdqVzLOYCzpXQgmOWNA25lY3FxyV1tROtV2XRcLMnHg-91Gn_PPk96CNn5vjfRj3PWApRQJWukfBbldaVEDSX-9ZJ8eIRejXPCJ-6pBgQackCKHyiXxpyT7_R1CoNJOw1M7wPVh0A1Bqr_BqpvUfT-3nq2g2__S_4liIA4ABmv4tanh9lP2N4BUwWrTw</recordid><startdate>20231201</startdate><enddate>20231201</enddate><creator>Zhao, Eryong</creator><creator>Gao, Kefei</creator><creator>Xiong, Jian</creator><creator>Liu, Zhihong</creator><creator>Chen, Yuelin</creator><creator>Yi, Lisha</creator><general>Springer Berlin Heidelberg</general><general>Springer Nature B.V</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>7TO</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope><scope>7S9</scope><scope>L.6</scope></search><sort><creationdate>20231201</creationdate><title>The roles of FXYD family members in ovarian cancer: an integrated analysis by mining TCGA and GEO databases and functional validations</title><author>Zhao, Eryong ; Gao, Kefei ; Xiong, Jian ; Liu, Zhihong ; Chen, Yuelin ; Yi, Lisha</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c408t-38390bbb2ea98a1b3babf65cd2211cb64c130b29c12b49b9b9242c8a3de569f23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Bioinformatics</topic><topic>biomarkers</topic><topic>Cancer Research</topic><topic>cell movement</topic><topic>Cell Movement - genetics</topic><topic>Chemotherapy</topic><topic>Correlation analysis</topic><topic>drug therapy</topic><topic>drugs</topic><topic>family</topic><topic>Female</topic><topic>Gene expression</topic><topic>gene ontology</topic><topic>Genes</topic><topic>genome</topic><topic>Genomes</topic><topic>Hematology</topic><topic>Humans</topic><topic>Internal Medicine</topic><topic>Invasiveness</topic><topic>Ion Channels</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Membrane Proteins - genetics</topic><topic>Membrane Proteins - metabolism</topic><topic>Metastases</topic><topic>metastasis</topic><topic>Microfilament Proteins - metabolism</topic><topic>neoplasm progression</topic><topic>Neoplasm Proteins - genetics</topic><topic>Oncology</topic><topic>Ovarian cancer</topic><topic>ovarian neoplasms</topic><topic>Ovarian Neoplasms - genetics</topic><topic>regression analysis</topic><topic>Signal transduction</topic><topic>Sodium-Potassium-Exchanging ATPase - genetics</topic><topic>Sodium-Potassium-Exchanging ATPase - metabolism</topic><topic>Therapeutic targets</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhao, Eryong</creatorcontrib><creatorcontrib>Gao, Kefei</creatorcontrib><creatorcontrib>Xiong, Jian</creatorcontrib><creatorcontrib>Liu, Zhihong</creatorcontrib><creatorcontrib>Chen, Yuelin</creatorcontrib><creatorcontrib>Yi, Lisha</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>Oncogenes and Growth Factors 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>Public Health Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</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>Research Library</collection><collection>Research Library (Corporate)</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 Basic</collection><collection>MEDLINE - Academic</collection><collection>AGRICOLA</collection><collection>AGRICOLA - Academic</collection><jtitle>Journal of cancer research and clinical oncology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhao, Eryong</au><au>Gao, Kefei</au><au>Xiong, Jian</au><au>Liu, Zhihong</au><au>Chen, Yuelin</au><au>Yi, Lisha</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The roles of FXYD family members in ovarian cancer: an integrated analysis by mining TCGA and GEO databases and functional validations</atitle><jtitle>Journal of cancer research and clinical oncology</jtitle><stitle>J Cancer Res Clin Oncol</stitle><addtitle>J Cancer Res Clin Oncol</addtitle><date>2023-12-01</date><risdate>2023</risdate><volume>149</volume><issue>19</issue><spage>17269</spage><epage>17284</epage><pages>17269-17284</pages><issn>0171-5216</issn><eissn>1432-1335</eissn><abstract>Background
The FXYD family of ion transport regulators have emerged as important modulators of cancer progression and metastasis. However, their expression and roles in ovarian cancer (OCa) have not been systematically investigated.
Methods
The expression of FXYD genes in OCa was analyzed using data from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO), as well as independent clinical samples. The prognostic values of FXYD genes were evaluated by Kaplan–Meier and Cox regression analysis. To explore potential mechanisms, bioinformatics approaches including Gene Ontology, KEGG pathway analysis, GSEA and drug sensitivity correlation analysis were performed. OCa cell lines overexpressing FXYD1, FXYD5 or FXYD7 were also generated and their impacts on proliferation, migration and invasion were assessed.
Results
FXYD1 and FXYD6 were significantly downregulated while FXYD3, FXYD4 and FXYD5 were upregulated in OCa tissues compared to normal tissues. FXYD1, FXYD5 and FXYD7 were independent adverse prognostic factors for OCa patients. Pathway and drug correlation analysis revealed that FXYD1, FXYD5 and FXYD7 genes regulated diverse oncogenic signaling cascades and modulated the response to various chemotherapeutic agents. Overexpression of FXYD1, FXYD5 or FXYD7 enhanced OCa cell motility and invasiveness in vitro.
Conclusion
Our results demonstrate aberrant expression patterns, prognostic values, and oncogenic activities of FXYD genes in OCa. FXYD1, FXYD5 and FXYD7 may serve as biomarkers and therapeutic targets for this disease. Targeting FXYD-mediated signaling represents a promising therapeutic strategy against OCa.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>37814066</pmid><doi>10.1007/s00432-023-05445-z</doi><tpages>16</tpages></addata></record> |
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| source | MEDLINE; Springer Nature - Complete Springer Journals |
| subjects | Bioinformatics biomarkers Cancer Research cell movement Cell Movement - genetics Chemotherapy Correlation analysis drug therapy drugs family Female Gene expression gene ontology Genes genome Genomes Hematology Humans Internal Medicine Invasiveness Ion Channels Medicine Medicine & Public Health Membrane Proteins - genetics Membrane Proteins - metabolism Metastases metastasis Microfilament Proteins - metabolism neoplasm progression Neoplasm Proteins - genetics Oncology Ovarian cancer ovarian neoplasms Ovarian Neoplasms - genetics regression analysis Signal transduction Sodium-Potassium-Exchanging ATPase - genetics Sodium-Potassium-Exchanging ATPase - metabolism Therapeutic targets |
| title | The roles of FXYD family members in ovarian cancer: an integrated analysis by mining TCGA and GEO databases and functional validations |
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