Expression and Role of CFTR in Human Esophageal Squamous Cell Carcinoma
Background The cystic fibrosis transmembrane conductance regulator (CFTR) is a cAMP-dependent chloride (Cl − ) anion conducting channel, and its role in esophageal squamous cell carcinoma (ESCC) was examined in the present study. Methods Overexpression experiments were conducted on human ESCC cell l...
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| Veröffentlicht in: | Annals of surgical oncology 2021-10, Vol.28 (11), p.6424-6436 |
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| creator | Matsumoto, Yoshihisa Shiozaki, Atsushi Kosuga, Toshiyuki Kudou, Michihiro Shimizu, Hiroki Arita, Tomohiro Konishi, Hirotaka Komatsu, Shuhei Kubota, Takeshi Fujiwara, Hitoshi Okamoto, Kazuma Kishimoto, Mitsuo Konishi, Eiichi Otsuji, Eigo |
| description | Background
The cystic fibrosis transmembrane conductance regulator (CFTR) is a cAMP-dependent chloride (Cl
−
) anion conducting channel, and its role in esophageal squamous cell carcinoma (ESCC) was examined in the present study.
Methods
Overexpression experiments were conducted on human ESCC cell lines following the transfection of a CFTR plasmid, and changes in cell proliferation, the cell cycle, apoptosis, migration, and invasion were assessed. A microarray analysis was performed to examine gene expression profiles. Fifty-three primary tumor samples collected from ESCC patients during esophagectomy were subjected to an immunohistochemical analysis.
Results
Transfection of the CFTR plasmid into the ESCC KYSE 170 and KYSE 70 cell lines suppressed cell proliferation, migration, and invasion and induced apoptosis. The microarray analysis showed the up-regulated expression of genes involved in the p38 signaling pathway in CFTR plasmid-transfected KYSE 170 cells. Immunohistochemical staining revealed a relationship between the CFTR expression pattern at the invasive front and the pN category. A relationship was also observed between the weak expression of CFTR at the invasive front and a shorter postoperative survival in a prognostic analysis.
Conclusions
The overexpression of CFTR in ESCC activated the p38 signaling pathway and was associated with a good patient prognosis. These results indicate the potential of CFTR as a mediator of and/or a biomarker for ESCC. |
| doi_str_mv | 10.1245/s10434-021-09752-y |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2501254010</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2501254010</sourcerecordid><originalsourceid>FETCH-LOGICAL-c525t-11a921852310bc67dc7041999f76356612a0ef28cd6eee1282a16dc433eb0fe03</originalsourceid><addsrcrecordid>eNp9kF1LwzAUhoMobn78AS8k4I031XOSJm0vpWxTGAh-XIesTWdH22zJCu7fG-1U8MKrhOQ573l5CLlAuEEWi1uPEPM4AoYRZIlg0e6AjFGEp1imeBjuINMoY1KMyIn3KwBMOIhjMuI8QRAQj8ls8r52xvvadlR3JX2yjaG2ovn05YnWHb3vW93RibfrN700uqHPm163tvc0N01Dc-2KurOtPiNHlW68Od-fp-R1OnnJ76P54-whv5tHhWBiGyHqjGEqGEdYFDIpiwRizLKsSiQXUiLTYCqWFqU0xiBLmUZZFjHnZgGVAX5KrofctbOb3vitamtfhCq6M6GVYgKQiRjwE736g65s77rQLlBJWMZTmQSKDVThrPfOVGrt6la7nUJQn5rVoFkFzepLs9qFoct9dL9oTfkz8u01AHwAfPjqlsb97v4n9gNAw4Wq</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2575663867</pqid></control><display><type>article</type><title>Expression and Role of CFTR in Human Esophageal Squamous Cell Carcinoma</title><source>MEDLINE</source><source>SpringerNature Journals</source><creator>Matsumoto, Yoshihisa ; Shiozaki, Atsushi ; Kosuga, Toshiyuki ; Kudou, Michihiro ; Shimizu, Hiroki ; Arita, Tomohiro ; Konishi, Hirotaka ; Komatsu, Shuhei ; Kubota, Takeshi ; Fujiwara, Hitoshi ; Okamoto, Kazuma ; Kishimoto, Mitsuo ; Konishi, Eiichi ; Otsuji, Eigo</creator><creatorcontrib>Matsumoto, Yoshihisa ; Shiozaki, Atsushi ; Kosuga, Toshiyuki ; Kudou, Michihiro ; Shimizu, Hiroki ; Arita, Tomohiro ; Konishi, Hirotaka ; Komatsu, Shuhei ; Kubota, Takeshi ; Fujiwara, Hitoshi ; Okamoto, Kazuma ; Kishimoto, Mitsuo ; Konishi, Eiichi ; Otsuji, Eigo</creatorcontrib><description>Background
The cystic fibrosis transmembrane conductance regulator (CFTR) is a cAMP-dependent chloride (Cl
−
) anion conducting channel, and its role in esophageal squamous cell carcinoma (ESCC) was examined in the present study.
Methods
Overexpression experiments were conducted on human ESCC cell lines following the transfection of a CFTR plasmid, and changes in cell proliferation, the cell cycle, apoptosis, migration, and invasion were assessed. A microarray analysis was performed to examine gene expression profiles. Fifty-three primary tumor samples collected from ESCC patients during esophagectomy were subjected to an immunohistochemical analysis.
Results
Transfection of the CFTR plasmid into the ESCC KYSE 170 and KYSE 70 cell lines suppressed cell proliferation, migration, and invasion and induced apoptosis. The microarray analysis showed the up-regulated expression of genes involved in the p38 signaling pathway in CFTR plasmid-transfected KYSE 170 cells. Immunohistochemical staining revealed a relationship between the CFTR expression pattern at the invasive front and the pN category. A relationship was also observed between the weak expression of CFTR at the invasive front and a shorter postoperative survival in a prognostic analysis.
Conclusions
The overexpression of CFTR in ESCC activated the p38 signaling pathway and was associated with a good patient prognosis. These results indicate the potential of CFTR as a mediator of and/or a biomarker for ESCC.</description><identifier>ISSN: 1068-9265</identifier><identifier>EISSN: 1534-4681</identifier><identifier>DOI: 10.1245/s10434-021-09752-y</identifier><identifier>PMID: 33710504</identifier><language>eng</language><publisher>Cham: Springer International Publishing</publisher><subject>Apoptosis ; Carcinoma, Squamous Cell - genetics ; Cell cycle ; Cell growth ; Cell Line, Tumor ; Cell migration ; Cell Movement ; Cell Proliferation ; Cystic fibrosis ; Cystic Fibrosis Transmembrane Conductance Regulator - genetics ; DNA microarrays ; Esophageal cancer ; Esophageal Neoplasms - genetics ; Esophageal Squamous Cell Carcinoma - genetics ; Esophagus ; Gene expression ; Gene Expression Regulation, Neoplastic ; Humans ; Invasiveness ; Medical prognosis ; Medicine ; Medicine & Public Health ; Oncology ; Signal transduction ; Squamous cell carcinoma ; Surgery ; Surgical Oncology ; Transfection ; Translational Research</subject><ispartof>Annals of surgical oncology, 2021-10, Vol.28 (11), p.6424-6436</ispartof><rights>Society of Surgical Oncology 2021</rights><rights>2021. Society of Surgical Oncology.</rights><rights>Society of Surgical Oncology 2021.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c525t-11a921852310bc67dc7041999f76356612a0ef28cd6eee1282a16dc433eb0fe03</citedby><cites>FETCH-LOGICAL-c525t-11a921852310bc67dc7041999f76356612a0ef28cd6eee1282a16dc433eb0fe03</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1245/s10434-021-09752-y$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1245/s10434-021-09752-y$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33710504$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Matsumoto, Yoshihisa</creatorcontrib><creatorcontrib>Shiozaki, Atsushi</creatorcontrib><creatorcontrib>Kosuga, Toshiyuki</creatorcontrib><creatorcontrib>Kudou, Michihiro</creatorcontrib><creatorcontrib>Shimizu, Hiroki</creatorcontrib><creatorcontrib>Arita, Tomohiro</creatorcontrib><creatorcontrib>Konishi, Hirotaka</creatorcontrib><creatorcontrib>Komatsu, Shuhei</creatorcontrib><creatorcontrib>Kubota, Takeshi</creatorcontrib><creatorcontrib>Fujiwara, Hitoshi</creatorcontrib><creatorcontrib>Okamoto, Kazuma</creatorcontrib><creatorcontrib>Kishimoto, Mitsuo</creatorcontrib><creatorcontrib>Konishi, Eiichi</creatorcontrib><creatorcontrib>Otsuji, Eigo</creatorcontrib><title>Expression and Role of CFTR in Human Esophageal Squamous Cell Carcinoma</title><title>Annals of surgical oncology</title><addtitle>Ann Surg Oncol</addtitle><addtitle>Ann Surg Oncol</addtitle><description>Background
The cystic fibrosis transmembrane conductance regulator (CFTR) is a cAMP-dependent chloride (Cl
−
) anion conducting channel, and its role in esophageal squamous cell carcinoma (ESCC) was examined in the present study.
Methods
Overexpression experiments were conducted on human ESCC cell lines following the transfection of a CFTR plasmid, and changes in cell proliferation, the cell cycle, apoptosis, migration, and invasion were assessed. A microarray analysis was performed to examine gene expression profiles. Fifty-three primary tumor samples collected from ESCC patients during esophagectomy were subjected to an immunohistochemical analysis.
Results
Transfection of the CFTR plasmid into the ESCC KYSE 170 and KYSE 70 cell lines suppressed cell proliferation, migration, and invasion and induced apoptosis. The microarray analysis showed the up-regulated expression of genes involved in the p38 signaling pathway in CFTR plasmid-transfected KYSE 170 cells. Immunohistochemical staining revealed a relationship between the CFTR expression pattern at the invasive front and the pN category. A relationship was also observed between the weak expression of CFTR at the invasive front and a shorter postoperative survival in a prognostic analysis.
Conclusions
The overexpression of CFTR in ESCC activated the p38 signaling pathway and was associated with a good patient prognosis. These results indicate the potential of CFTR as a mediator of and/or a biomarker for ESCC.</description><subject>Apoptosis</subject><subject>Carcinoma, Squamous Cell - genetics</subject><subject>Cell cycle</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell migration</subject><subject>Cell Movement</subject><subject>Cell Proliferation</subject><subject>Cystic fibrosis</subject><subject>Cystic Fibrosis Transmembrane Conductance Regulator - genetics</subject><subject>DNA microarrays</subject><subject>Esophageal cancer</subject><subject>Esophageal Neoplasms - genetics</subject><subject>Esophageal Squamous Cell Carcinoma - genetics</subject><subject>Esophagus</subject><subject>Gene expression</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Humans</subject><subject>Invasiveness</subject><subject>Medical prognosis</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Oncology</subject><subject>Signal transduction</subject><subject>Squamous cell carcinoma</subject><subject>Surgery</subject><subject>Surgical Oncology</subject><subject>Transfection</subject><subject>Translational Research</subject><issn>1068-9265</issn><issn>1534-4681</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNp9kF1LwzAUhoMobn78AS8k4I031XOSJm0vpWxTGAh-XIesTWdH22zJCu7fG-1U8MKrhOQ573l5CLlAuEEWi1uPEPM4AoYRZIlg0e6AjFGEp1imeBjuINMoY1KMyIn3KwBMOIhjMuI8QRAQj8ls8r52xvvadlR3JX2yjaG2ovn05YnWHb3vW93RibfrN700uqHPm163tvc0N01Dc-2KurOtPiNHlW68Od-fp-R1OnnJ76P54-whv5tHhWBiGyHqjGEqGEdYFDIpiwRizLKsSiQXUiLTYCqWFqU0xiBLmUZZFjHnZgGVAX5KrofctbOb3vitamtfhCq6M6GVYgKQiRjwE736g65s77rQLlBJWMZTmQSKDVThrPfOVGrt6la7nUJQn5rVoFkFzepLs9qFoct9dL9oTfkz8u01AHwAfPjqlsb97v4n9gNAw4Wq</recordid><startdate>20211001</startdate><enddate>20211001</enddate><creator>Matsumoto, Yoshihisa</creator><creator>Shiozaki, Atsushi</creator><creator>Kosuga, Toshiyuki</creator><creator>Kudou, Michihiro</creator><creator>Shimizu, Hiroki</creator><creator>Arita, Tomohiro</creator><creator>Konishi, Hirotaka</creator><creator>Komatsu, Shuhei</creator><creator>Kubota, Takeshi</creator><creator>Fujiwara, Hitoshi</creator><creator>Okamoto, Kazuma</creator><creator>Kishimoto, Mitsuo</creator><creator>Konishi, Eiichi</creator><creator>Otsuji, Eigo</creator><general>Springer International Publishing</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>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>7X8</scope></search><sort><creationdate>20211001</creationdate><title>Expression and Role of CFTR in Human Esophageal Squamous Cell Carcinoma</title><author>Matsumoto, Yoshihisa ; Shiozaki, Atsushi ; Kosuga, Toshiyuki ; Kudou, Michihiro ; Shimizu, Hiroki ; Arita, Tomohiro ; Konishi, Hirotaka ; Komatsu, Shuhei ; Kubota, Takeshi ; Fujiwara, Hitoshi ; Okamoto, Kazuma ; Kishimoto, Mitsuo ; Konishi, Eiichi ; Otsuji, Eigo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c525t-11a921852310bc67dc7041999f76356612a0ef28cd6eee1282a16dc433eb0fe03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Apoptosis</topic><topic>Carcinoma, Squamous Cell - genetics</topic><topic>Cell cycle</topic><topic>Cell growth</topic><topic>Cell Line, Tumor</topic><topic>Cell migration</topic><topic>Cell Movement</topic><topic>Cell Proliferation</topic><topic>Cystic fibrosis</topic><topic>Cystic Fibrosis Transmembrane Conductance Regulator - genetics</topic><topic>DNA microarrays</topic><topic>Esophageal cancer</topic><topic>Esophageal Neoplasms - genetics</topic><topic>Esophageal Squamous Cell Carcinoma - genetics</topic><topic>Esophagus</topic><topic>Gene expression</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Humans</topic><topic>Invasiveness</topic><topic>Medical prognosis</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Oncology</topic><topic>Signal transduction</topic><topic>Squamous cell carcinoma</topic><topic>Surgery</topic><topic>Surgical Oncology</topic><topic>Transfection</topic><topic>Translational Research</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Matsumoto, Yoshihisa</creatorcontrib><creatorcontrib>Shiozaki, Atsushi</creatorcontrib><creatorcontrib>Kosuga, Toshiyuki</creatorcontrib><creatorcontrib>Kudou, Michihiro</creatorcontrib><creatorcontrib>Shimizu, Hiroki</creatorcontrib><creatorcontrib>Arita, Tomohiro</creatorcontrib><creatorcontrib>Konishi, Hirotaka</creatorcontrib><creatorcontrib>Komatsu, Shuhei</creatorcontrib><creatorcontrib>Kubota, Takeshi</creatorcontrib><creatorcontrib>Fujiwara, Hitoshi</creatorcontrib><creatorcontrib>Okamoto, Kazuma</creatorcontrib><creatorcontrib>Kishimoto, Mitsuo</creatorcontrib><creatorcontrib>Konishi, Eiichi</creatorcontrib><creatorcontrib>Otsuji, Eigo</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>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>MEDLINE - Academic</collection><jtitle>Annals of surgical oncology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Matsumoto, Yoshihisa</au><au>Shiozaki, Atsushi</au><au>Kosuga, Toshiyuki</au><au>Kudou, Michihiro</au><au>Shimizu, Hiroki</au><au>Arita, Tomohiro</au><au>Konishi, Hirotaka</au><au>Komatsu, Shuhei</au><au>Kubota, Takeshi</au><au>Fujiwara, Hitoshi</au><au>Okamoto, Kazuma</au><au>Kishimoto, Mitsuo</au><au>Konishi, Eiichi</au><au>Otsuji, Eigo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Expression and Role of CFTR in Human Esophageal Squamous Cell Carcinoma</atitle><jtitle>Annals of surgical oncology</jtitle><stitle>Ann Surg Oncol</stitle><addtitle>Ann Surg Oncol</addtitle><date>2021-10-01</date><risdate>2021</risdate><volume>28</volume><issue>11</issue><spage>6424</spage><epage>6436</epage><pages>6424-6436</pages><issn>1068-9265</issn><eissn>1534-4681</eissn><abstract>Background
The cystic fibrosis transmembrane conductance regulator (CFTR) is a cAMP-dependent chloride (Cl
−
) anion conducting channel, and its role in esophageal squamous cell carcinoma (ESCC) was examined in the present study.
Methods
Overexpression experiments were conducted on human ESCC cell lines following the transfection of a CFTR plasmid, and changes in cell proliferation, the cell cycle, apoptosis, migration, and invasion were assessed. A microarray analysis was performed to examine gene expression profiles. Fifty-three primary tumor samples collected from ESCC patients during esophagectomy were subjected to an immunohistochemical analysis.
Results
Transfection of the CFTR plasmid into the ESCC KYSE 170 and KYSE 70 cell lines suppressed cell proliferation, migration, and invasion and induced apoptosis. The microarray analysis showed the up-regulated expression of genes involved in the p38 signaling pathway in CFTR plasmid-transfected KYSE 170 cells. Immunohistochemical staining revealed a relationship between the CFTR expression pattern at the invasive front and the pN category. A relationship was also observed between the weak expression of CFTR at the invasive front and a shorter postoperative survival in a prognostic analysis.
Conclusions
The overexpression of CFTR in ESCC activated the p38 signaling pathway and was associated with a good patient prognosis. These results indicate the potential of CFTR as a mediator of and/or a biomarker for ESCC.</abstract><cop>Cham</cop><pub>Springer International Publishing</pub><pmid>33710504</pmid><doi>10.1245/s10434-021-09752-y</doi><tpages>13</tpages></addata></record> |
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| ispartof | Annals of surgical oncology, 2021-10, Vol.28 (11), p.6424-6436 |
| issn | 1068-9265 1534-4681 |
| language | eng |
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| source | MEDLINE; SpringerNature Journals |
| subjects | Apoptosis Carcinoma, Squamous Cell - genetics Cell cycle Cell growth Cell Line, Tumor Cell migration Cell Movement Cell Proliferation Cystic fibrosis Cystic Fibrosis Transmembrane Conductance Regulator - genetics DNA microarrays Esophageal cancer Esophageal Neoplasms - genetics Esophageal Squamous Cell Carcinoma - genetics Esophagus Gene expression Gene Expression Regulation, Neoplastic Humans Invasiveness Medical prognosis Medicine Medicine & Public Health Oncology Signal transduction Squamous cell carcinoma Surgery Surgical Oncology Transfection Translational Research |
| title | Expression and Role of CFTR in Human Esophageal Squamous Cell Carcinoma |
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