CAF-secreted CXCL1 conferred radioresistance by regulating DNA damage response in a ROS-dependent manner in esophageal squamous cell carcinoma
Five-year survival rate of esophageal squamous cell carcinoma (ESCC) patients treated with radiotherapy is
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| Veröffentlicht in: | Cell death & disease 2017-05, Vol.8 (5), p.e2790-e2790 |
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| container_title | Cell death & disease |
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| creator | Zhang, Hongfang Yue, Jing Jiang, Zhenzhen Zhou, Rongjing Xie, Ruifei Xu, Yiping Wu, Shixiu |
| description | Five-year survival rate of esophageal squamous cell carcinoma (ESCC) patients treated with radiotherapy is |
| doi_str_mv | 10.1038/cddis.2017.180 |
| format | Article |
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in vitro
and
in vivo
. CAF-secreted CXCL1 inhibited the expression of reactive oxygen species (ROS)-scavenging enzyme superoxide dismutase 1, leading to increased ROS accumulation following radiation, by which DNA damage repair was enhanced and the radioresistance was mediated. CAF-secreted CXCL1 mediated the radioresistance also by activation of Mek/Erk pathway. The cross talk of CAFs and ESCC cells induced CXCL1 expression in an autocrine/paracrine signaling loop, which further enhanced tumor radioresistance. Together, our study highlighted CAF-secreted CXCL1 as an attractive target to reverse tumor radioresistance and can be used as an independent prognostic factor of ESCC patients treated with chemoradiotherapy.</description><identifier>ISSN: 2041-4889</identifier><identifier>EISSN: 2041-4889</identifier><identifier>DOI: 10.1038/cddis.2017.180</identifier><identifier>PMID: 28518141</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13/1 ; 13/21 ; 13/51 ; 13/95 ; 14/19 ; 38/77 ; 631/337/1427/2566 ; 631/67/1059/2326 ; 631/80/86 ; 64/60 ; 692/699/67/1504/1477 ; 82/80 ; Antibodies ; Ataxia Telangiectasia Mutated Proteins - metabolism ; Autocrine signalling ; Biochemistry ; Biomedical and Life Sciences ; Cancer-Associated Fibroblasts - metabolism ; Carcinoma, Squamous Cell - drug therapy ; Carcinoma, Squamous Cell - metabolism ; Carcinoma, Squamous Cell - pathology ; Carcinoma, Squamous Cell - radiotherapy ; Cell Biology ; Cell Culture ; Cell Line, Tumor ; Chemokine CXCL1 - metabolism ; Chemokines ; Chemoradiotherapy ; DNA Damage ; DNA Repair ; Esophageal cancer ; Esophageal Neoplasms - drug therapy ; Esophageal Neoplasms - metabolism ; Esophageal Neoplasms - pathology ; Esophageal Neoplasms - radiotherapy ; Esophageal Squamous Cell Carcinoma ; Esophagus ; Extracellular Signal-Regulated MAP Kinases - metabolism ; Female ; Fibroblasts ; Humans ; Immunology ; Life Sciences ; Male ; Metabolic pathways ; Middle Aged ; Mitogen-Activated Protein Kinase Kinases - metabolism ; Original ; original-article ; Paracrine Communication ; Paracrine signalling ; Prognosis ; Radiation therapy ; Radiation Tolerance ; Radioresistance ; Reactive oxygen species ; Reactive Oxygen Species - metabolism ; Signal Transduction ; Squamous cell carcinoma ; Superoxide dismutase ; Superoxide Dismutase - metabolism ; Survival ; Survival Analysis ; Xenograft Model Antitumor Assays</subject><ispartof>Cell death & disease, 2017-05, Vol.8 (5), p.e2790-e2790</ispartof><rights>The Author(s) 2017</rights><rights>Copyright Nature Publishing Group May 2017</rights><rights>Copyright © 2017 The Author(s) 2017 The Author(s)</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c524t-7046272ed90ce91edb83ba0f4078c1d31b9594035e6673f88d8aabb108a197773</citedby><cites>FETCH-LOGICAL-c524t-7046272ed90ce91edb83ba0f4078c1d31b9594035e6673f88d8aabb108a197773</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5520705/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5520705/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27901,27902,41096,42165,51551,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28518141$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, Hongfang</creatorcontrib><creatorcontrib>Yue, Jing</creatorcontrib><creatorcontrib>Jiang, Zhenzhen</creatorcontrib><creatorcontrib>Zhou, Rongjing</creatorcontrib><creatorcontrib>Xie, Ruifei</creatorcontrib><creatorcontrib>Xu, Yiping</creatorcontrib><creatorcontrib>Wu, Shixiu</creatorcontrib><title>CAF-secreted CXCL1 conferred radioresistance by regulating DNA damage response in a ROS-dependent manner in esophageal squamous cell carcinoma</title><title>Cell death & disease</title><addtitle>Cell Death Dis</addtitle><addtitle>Cell Death Dis</addtitle><description>Five-year survival rate of esophageal squamous cell carcinoma (ESCC) patients treated with radiotherapy is <20%. Our study aimed to investigate whether cancer-associated fibroblasts (CAFs), one major component of tumor microenvironment, were involved in tumor radioresistance in ESCC. By use of human chemokine/cytokine array, human chemokine CXCL1 was found to be highly expressed in CAFs compared with that in matched normal fibroblasts. Inhibition of CXCL1 expression in CAFs significantly reversed CAF-conferred radioresistance
in vitro
and
in vivo
. CAF-secreted CXCL1 inhibited the expression of reactive oxygen species (ROS)-scavenging enzyme superoxide dismutase 1, leading to increased ROS accumulation following radiation, by which DNA damage repair was enhanced and the radioresistance was mediated. CAF-secreted CXCL1 mediated the radioresistance also by activation of Mek/Erk pathway. The cross talk of CAFs and ESCC cells induced CXCL1 expression in an autocrine/paracrine signaling loop, which further enhanced tumor radioresistance. Together, our study highlighted CAF-secreted CXCL1 as an attractive target to reverse tumor radioresistance and can be used as an independent prognostic factor of ESCC patients treated with chemoradiotherapy.</description><subject>13/1</subject><subject>13/21</subject><subject>13/51</subject><subject>13/95</subject><subject>14/19</subject><subject>38/77</subject><subject>631/337/1427/2566</subject><subject>631/67/1059/2326</subject><subject>631/80/86</subject><subject>64/60</subject><subject>692/699/67/1504/1477</subject><subject>82/80</subject><subject>Antibodies</subject><subject>Ataxia Telangiectasia Mutated Proteins - metabolism</subject><subject>Autocrine signalling</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Cancer-Associated Fibroblasts - metabolism</subject><subject>Carcinoma, Squamous Cell - drug therapy</subject><subject>Carcinoma, Squamous Cell - metabolism</subject><subject>Carcinoma, Squamous Cell - pathology</subject><subject>Carcinoma, Squamous Cell - radiotherapy</subject><subject>Cell Biology</subject><subject>Cell Culture</subject><subject>Cell Line, Tumor</subject><subject>Chemokine CXCL1 - metabolism</subject><subject>Chemokines</subject><subject>Chemoradiotherapy</subject><subject>DNA Damage</subject><subject>DNA Repair</subject><subject>Esophageal cancer</subject><subject>Esophageal Neoplasms - drug therapy</subject><subject>Esophageal Neoplasms - metabolism</subject><subject>Esophageal Neoplasms - pathology</subject><subject>Esophageal Neoplasms - radiotherapy</subject><subject>Esophageal Squamous Cell Carcinoma</subject><subject>Esophagus</subject><subject>Extracellular Signal-Regulated MAP Kinases - metabolism</subject><subject>Female</subject><subject>Fibroblasts</subject><subject>Humans</subject><subject>Immunology</subject><subject>Life Sciences</subject><subject>Male</subject><subject>Metabolic pathways</subject><subject>Middle Aged</subject><subject>Mitogen-Activated Protein Kinase Kinases - metabolism</subject><subject>Original</subject><subject>original-article</subject><subject>Paracrine Communication</subject><subject>Paracrine signalling</subject><subject>Prognosis</subject><subject>Radiation therapy</subject><subject>Radiation Tolerance</subject><subject>Radioresistance</subject><subject>Reactive oxygen species</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Signal Transduction</subject><subject>Squamous cell carcinoma</subject><subject>Superoxide dismutase</subject><subject>Superoxide Dismutase - metabolism</subject><subject>Survival</subject><subject>Survival Analysis</subject><subject>Xenograft Model Antitumor Assays</subject><issn>2041-4889</issn><issn>2041-4889</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNptkUtv1DAUhSMEolXpliWyxIZNprbzsLNBGqUUkEZU4iGxs27sm9RVYqd2gtQ_wW_Gw5RqQHjjx_3u8T06WfaS0Q2jhbzQxti44ZSJDZP0SXbKacnyUsrm6dH5JDuP8ZamVRSUV_Xz7ITLiklWstPsZ7u9yiPqgAsa0n5vd4xo73oMId0DGOsDRhsXcBpJd08CDusIi3UDufy0JQYmGDC9xtm7iMQ6AuTz9Zfc4IzOoFvIBM5h2Fcw-vkm4TCSeLfC5NdINI4j0RC0dX6CF9mzHsaI5w_7Wfbt6t3X9kO-u37_sd3ucl3xcskFLWsuOJqGamwYmk4WHdC-pEJqZgrWNVVT0qLCuhZFL6WRAF3HqATWCCGKs-ztQXdeuwmNTnMGGNUc7AThXnmw6u-Kszdq8D9UVXEqaJUE3jwIBH-3YlzUZOPeCzhMthRrKGW8rnmd0Nf_oLd-DS7ZSxQTgkveFInaHCgdfIwB-8dhGFX7tNXvtNU-bZXSTg2vji084n-yTcDFAYip5AYMR__-X_IXEo63CQ</recordid><startdate>20170518</startdate><enddate>20170518</enddate><creator>Zhang, Hongfang</creator><creator>Yue, Jing</creator><creator>Jiang, Zhenzhen</creator><creator>Zhou, Rongjing</creator><creator>Xie, Ruifei</creator><creator>Xu, Yiping</creator><creator>Wu, Shixiu</creator><general>Nature Publishing Group UK</general><general>Springer Nature B.V</general><general>Nature Publishing Group</general><scope>C6C</scope><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>88A</scope><scope>88I</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M2P</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20170518</creationdate><title>CAF-secreted CXCL1 conferred radioresistance by regulating DNA damage response in a ROS-dependent manner in esophageal squamous cell carcinoma</title><author>Zhang, Hongfang ; Yue, Jing ; Jiang, Zhenzhen ; Zhou, Rongjing ; Xie, Ruifei ; Xu, Yiping ; Wu, Shixiu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c524t-7046272ed90ce91edb83ba0f4078c1d31b9594035e6673f88d8aabb108a197773</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>13/1</topic><topic>13/21</topic><topic>13/51</topic><topic>13/95</topic><topic>14/19</topic><topic>38/77</topic><topic>631/337/1427/2566</topic><topic>631/67/1059/2326</topic><topic>631/80/86</topic><topic>64/60</topic><topic>692/699/67/1504/1477</topic><topic>82/80</topic><topic>Antibodies</topic><topic>Ataxia Telangiectasia Mutated Proteins - metabolism</topic><topic>Autocrine signalling</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Cancer-Associated Fibroblasts - metabolism</topic><topic>Carcinoma, Squamous Cell - drug therapy</topic><topic>Carcinoma, Squamous Cell - metabolism</topic><topic>Carcinoma, Squamous Cell - pathology</topic><topic>Carcinoma, Squamous Cell - radiotherapy</topic><topic>Cell Biology</topic><topic>Cell Culture</topic><topic>Cell Line, Tumor</topic><topic>Chemokine CXCL1 - metabolism</topic><topic>Chemokines</topic><topic>Chemoradiotherapy</topic><topic>DNA Damage</topic><topic>DNA Repair</topic><topic>Esophageal cancer</topic><topic>Esophageal Neoplasms - drug therapy</topic><topic>Esophageal Neoplasms - metabolism</topic><topic>Esophageal Neoplasms - pathology</topic><topic>Esophageal Neoplasms - radiotherapy</topic><topic>Esophageal Squamous Cell Carcinoma</topic><topic>Esophagus</topic><topic>Extracellular Signal-Regulated MAP Kinases - metabolism</topic><topic>Female</topic><topic>Fibroblasts</topic><topic>Humans</topic><topic>Immunology</topic><topic>Life Sciences</topic><topic>Male</topic><topic>Metabolic pathways</topic><topic>Middle Aged</topic><topic>Mitogen-Activated Protein Kinase Kinases - metabolism</topic><topic>Original</topic><topic>original-article</topic><topic>Paracrine Communication</topic><topic>Paracrine signalling</topic><topic>Prognosis</topic><topic>Radiation therapy</topic><topic>Radiation Tolerance</topic><topic>Radioresistance</topic><topic>Reactive oxygen species</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Signal Transduction</topic><topic>Squamous cell carcinoma</topic><topic>Superoxide dismutase</topic><topic>Superoxide Dismutase - metabolism</topic><topic>Survival</topic><topic>Survival Analysis</topic><topic>Xenograft Model Antitumor Assays</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhang, Hongfang</creatorcontrib><creatorcontrib>Yue, Jing</creatorcontrib><creatorcontrib>Jiang, Zhenzhen</creatorcontrib><creatorcontrib>Zhou, Rongjing</creatorcontrib><creatorcontrib>Xie, Ruifei</creatorcontrib><creatorcontrib>Xu, Yiping</creatorcontrib><creatorcontrib>Wu, Shixiu</creatorcontrib><collection>Springer Nature OA Free Journals</collection><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>Biology Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science 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 Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</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>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Publicly Available Content 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>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cell death & disease</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, Hongfang</au><au>Yue, Jing</au><au>Jiang, Zhenzhen</au><au>Zhou, Rongjing</au><au>Xie, Ruifei</au><au>Xu, Yiping</au><au>Wu, Shixiu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>CAF-secreted CXCL1 conferred radioresistance by regulating DNA damage response in a ROS-dependent manner in esophageal squamous cell carcinoma</atitle><jtitle>Cell death & disease</jtitle><stitle>Cell Death Dis</stitle><addtitle>Cell Death Dis</addtitle><date>2017-05-18</date><risdate>2017</risdate><volume>8</volume><issue>5</issue><spage>e2790</spage><epage>e2790</epage><pages>e2790-e2790</pages><issn>2041-4889</issn><eissn>2041-4889</eissn><abstract>Five-year survival rate of esophageal squamous cell carcinoma (ESCC) patients treated with radiotherapy is <20%. Our study aimed to investigate whether cancer-associated fibroblasts (CAFs), one major component of tumor microenvironment, were involved in tumor radioresistance in ESCC. By use of human chemokine/cytokine array, human chemokine CXCL1 was found to be highly expressed in CAFs compared with that in matched normal fibroblasts. Inhibition of CXCL1 expression in CAFs significantly reversed CAF-conferred radioresistance
in vitro
and
in vivo
. CAF-secreted CXCL1 inhibited the expression of reactive oxygen species (ROS)-scavenging enzyme superoxide dismutase 1, leading to increased ROS accumulation following radiation, by which DNA damage repair was enhanced and the radioresistance was mediated. CAF-secreted CXCL1 mediated the radioresistance also by activation of Mek/Erk pathway. The cross talk of CAFs and ESCC cells induced CXCL1 expression in an autocrine/paracrine signaling loop, which further enhanced tumor radioresistance. Together, our study highlighted CAF-secreted CXCL1 as an attractive target to reverse tumor radioresistance and can be used as an independent prognostic factor of ESCC patients treated with chemoradiotherapy.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>28518141</pmid><doi>10.1038/cddis.2017.180</doi><oa>free_for_read</oa></addata></record> |
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| subjects | 13/1 13/21 13/51 13/95 14/19 38/77 631/337/1427/2566 631/67/1059/2326 631/80/86 64/60 692/699/67/1504/1477 82/80 Antibodies Ataxia Telangiectasia Mutated Proteins - metabolism Autocrine signalling Biochemistry Biomedical and Life Sciences Cancer-Associated Fibroblasts - metabolism Carcinoma, Squamous Cell - drug therapy Carcinoma, Squamous Cell - metabolism Carcinoma, Squamous Cell - pathology Carcinoma, Squamous Cell - radiotherapy Cell Biology Cell Culture Cell Line, Tumor Chemokine CXCL1 - metabolism Chemokines Chemoradiotherapy DNA Damage DNA Repair Esophageal cancer Esophageal Neoplasms - drug therapy Esophageal Neoplasms - metabolism Esophageal Neoplasms - pathology Esophageal Neoplasms - radiotherapy Esophageal Squamous Cell Carcinoma Esophagus Extracellular Signal-Regulated MAP Kinases - metabolism Female Fibroblasts Humans Immunology Life Sciences Male Metabolic pathways Middle Aged Mitogen-Activated Protein Kinase Kinases - metabolism Original original-article Paracrine Communication Paracrine signalling Prognosis Radiation therapy Radiation Tolerance Radioresistance Reactive oxygen species Reactive Oxygen Species - metabolism Signal Transduction Squamous cell carcinoma Superoxide dismutase Superoxide Dismutase - metabolism Survival Survival Analysis Xenograft Model Antitumor Assays |
| title | CAF-secreted CXCL1 conferred radioresistance by regulating DNA damage response in a ROS-dependent manner in esophageal squamous cell carcinoma |
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