HOXB7 mediates cisplatin resistance in esophageal squamous cell carcinoma through involvement of DNA damage repair
Background DNA damage repair is an important mechanism of platinum resistance. HOXB7 is one member of HOX family genes, which are essential developmental regulators and frequently dysregulated in cancer. Recently, its relevance in chemotherapy resistance and DNA damage repair has also been addressed...
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| Veröffentlicht in: | Thoracic cancer 2020-11, Vol.11 (11), p.3071-3085 |
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| creator | Zhou, Ting Fu, Hao Dong, Bin Dai, Liang Yang, Yongbo Yan, Wanpu Shen, Luyan |
| description | Background
DNA damage repair is an important mechanism of platinum resistance. HOXB7 is one member of HOX family genes, which are essential developmental regulators and frequently dysregulated in cancer. Recently, its relevance in chemotherapy resistance and DNA damage repair has also been addressed. However, little is known regarding the association between HOXB7 and chemotherapy resistance in esophageal squamous cell carcinoma (ESCC).
Methods
The association between HOXB7 expression detected by immunohistochemisty and tumor regression grade (TRG) and long‐term survival was analyzed in 143 ESCC patients who underwent neoadjuvant chemotherapy. CCK8 assay was used to examine the effect of cisplatin in a panel of four ESCC cell lines. A stable cell strain with HOXB7 knockdown of KYSE150 and KYSE450 was established to explore the effect on cisplatin sensitivity. The interaction of HOXB7 with Ku70, Ku80 and DNA‐PKcs was determined by GST‐pull down, coimmunoprecipitation and immunofluorescent colocalization. Finally, we investigated whether disrupting HOXB7 function by a synthetic peptide HXR9 blocking the formation of HOXB7/PBX could enhance cisplatin sensitivity in vitro and in vivo.
Results
High expression of HOXB7 was associated with cisplatin resistance and worse chemotherapy efficacy. HOXB7 knockdown reinforced cisplatin sensitivity. It was identified that HOXB7 interacts with Ku70, Ku80 and DNA‐PKcs. HOXB7 knockdown was related to the downregulation of Ku70, Ku80 and DNA‐PKcs as well as arrested cell cycle in S phase. HOXB7 inhibition by HXR9 had a synergistic effect to improve cisplatin sensitivity.
Conclusion
HOXB7 may be a biomarker for the prediction of chemoresistance of ESCC and serves as a promising therapeutic target. |
| doi_str_mv | 10.1111/1759-7714.13142 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_crossref_primary_10_1111_1759_7714_13142</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><doaj_id>oai_doaj_org_article_4c69cd2bf8484e39aee2e5c54db16bf0</doaj_id><sourcerecordid>2456547911</sourcerecordid><originalsourceid>FETCH-LOGICAL-c5992-36b1aaef423cf1979b82c581b78806b6830796e3b858e4e2c31a6be699106e7e3</originalsourceid><addsrcrecordid>eNqNkk1v1DAQhiMEolXpmRuKxBFtaye2Y1-QlkA_pIpeisTNsp3JrldJnNrJov57ZrvLip5gLv565vWMX2fZe0ouKMYlrbhaVBVlF7SkrHiVnR53Xh_nRJxk5yltCEYpFSn42-ykpFxIwflpFm_uf36p8h4abyZIufNp7MzkhzxC8mkyg4McV5DCuDYrMF2eHmfThxlZ6Lrcmej8EHqTT-sY5tUa6W3ottDDMOWhzb9-X-aN6TEXJUfj47vsTWu6BOeH8Sz7cfXtob5Z3N1f39bLu4XjShWLUlhqDLSsKF1LVaWsLByX1FZSEmGFLEmlBJRWcgkMCldSIywIpSgRUEF5lt3udZtgNnqMvjfxSQfj9fNGiCtt4uRdB5o5oVxT2FYyyaBUBqAA7jhrLBW2Jaj1ea81zhbfymFv0XQvRF-eDH6tV2GrK0EEoRwFPh4EYnicIU16E-Y4YP-6YFxwVilKkbrcUy6GlCK0xxso0TvP9c5VvXNYP3uOGR_-LuzI_3EYgU974BfY0CbnAR09YvgpmFSswDIxdgXI_6drP-FPCUMd5mHCVH5I9R08_atw_VAv9x38BtLv2AU</addsrcrecordid><sourcetype>Open Website</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2456547911</pqid></control><display><type>article</type><title>HOXB7 mediates cisplatin resistance in esophageal squamous cell carcinoma through involvement of DNA damage repair</title><source>DOAJ Directory of Open Access Journals</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Access via Wiley Online Library</source><source>Web of Science - Science Citation Index Expanded - 2020<img src="https://exlibris-pub.s3.amazonaws.com/fromwos-v2.jpg" /></source><source>Wiley Online Library (Open Access Collection)</source><source>PubMed Central</source><creator>Zhou, Ting ; Fu, Hao ; Dong, Bin ; Dai, Liang ; Yang, Yongbo ; Yan, Wanpu ; Shen, Luyan</creator><creatorcontrib>Zhou, Ting ; Fu, Hao ; Dong, Bin ; Dai, Liang ; Yang, Yongbo ; Yan, Wanpu ; Shen, Luyan</creatorcontrib><description>Background
DNA damage repair is an important mechanism of platinum resistance. HOXB7 is one member of HOX family genes, which are essential developmental regulators and frequently dysregulated in cancer. Recently, its relevance in chemotherapy resistance and DNA damage repair has also been addressed. However, little is known regarding the association between HOXB7 and chemotherapy resistance in esophageal squamous cell carcinoma (ESCC).
Methods
The association between HOXB7 expression detected by immunohistochemisty and tumor regression grade (TRG) and long‐term survival was analyzed in 143 ESCC patients who underwent neoadjuvant chemotherapy. CCK8 assay was used to examine the effect of cisplatin in a panel of four ESCC cell lines. A stable cell strain with HOXB7 knockdown of KYSE150 and KYSE450 was established to explore the effect on cisplatin sensitivity. The interaction of HOXB7 with Ku70, Ku80 and DNA‐PKcs was determined by GST‐pull down, coimmunoprecipitation and immunofluorescent colocalization. Finally, we investigated whether disrupting HOXB7 function by a synthetic peptide HXR9 blocking the formation of HOXB7/PBX could enhance cisplatin sensitivity in vitro and in vivo.
Results
High expression of HOXB7 was associated with cisplatin resistance and worse chemotherapy efficacy. HOXB7 knockdown reinforced cisplatin sensitivity. It was identified that HOXB7 interacts with Ku70, Ku80 and DNA‐PKcs. HOXB7 knockdown was related to the downregulation of Ku70, Ku80 and DNA‐PKcs as well as arrested cell cycle in S phase. HOXB7 inhibition by HXR9 had a synergistic effect to improve cisplatin sensitivity.
Conclusion
HOXB7 may be a biomarker for the prediction of chemoresistance of ESCC and serves as a promising therapeutic target.</description><identifier>ISSN: 1759-7706</identifier><identifier>EISSN: 1759-7714</identifier><identifier>DOI: 10.1111/1759-7714.13142</identifier><identifier>PMID: 31568655</identifier><language>eng</language><publisher>Melbourne: John Wiley & Sons Australia, Ltd</publisher><subject>Antibodies ; Antigens ; Apoptosis ; Cancer therapies ; Cell cycle ; Chemoresistance ; Chemotherapy ; Deoxyribonucleic acid ; DNA ; DNA damage ; DNA repair ; Drug resistance ; ESCC ; Esophageal cancer ; homeobox gene ; Kinases ; Life Sciences & Biomedicine ; NHEJ ; Oncology ; Original ; Respiratory System ; Science & Technology ; Squamous cell carcinoma ; Tumors</subject><ispartof>Thoracic cancer, 2020-11, Vol.11 (11), p.3071-3085</ispartof><rights>2019 The Authors. Thoracic Cancer published by China Lung Oncology Group and John Wiley & Sons Australia, Ltd</rights><rights>2019 The Authors. Thoracic Cancer published by China Lung Oncology Group and John Wiley & Sons Australia, Ltd.</rights><rights>2020. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>true</woscitedreferencessubscribed><woscitedreferencescount>27</woscitedreferencescount><woscitedreferencesoriginalsourcerecordid>wos000489427600001</woscitedreferencesoriginalsourcerecordid><citedby>FETCH-LOGICAL-c5992-36b1aaef423cf1979b82c581b78806b6830796e3b858e4e2c31a6be699106e7e3</citedby><cites>FETCH-LOGICAL-c5992-36b1aaef423cf1979b82c581b78806b6830796e3b858e4e2c31a6be699106e7e3</cites><orcidid>0000-0003-4573-9872</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7606015/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7606015/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,729,782,786,866,887,1419,2104,2116,11569,27931,27932,28255,45581,45582,46059,46483,53798,53800</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31568655$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhou, Ting</creatorcontrib><creatorcontrib>Fu, Hao</creatorcontrib><creatorcontrib>Dong, Bin</creatorcontrib><creatorcontrib>Dai, Liang</creatorcontrib><creatorcontrib>Yang, Yongbo</creatorcontrib><creatorcontrib>Yan, Wanpu</creatorcontrib><creatorcontrib>Shen, Luyan</creatorcontrib><title>HOXB7 mediates cisplatin resistance in esophageal squamous cell carcinoma through involvement of DNA damage repair</title><title>Thoracic cancer</title><addtitle>THORAC CANCER</addtitle><addtitle>Thorac Cancer</addtitle><description>Background
DNA damage repair is an important mechanism of platinum resistance. HOXB7 is one member of HOX family genes, which are essential developmental regulators and frequently dysregulated in cancer. Recently, its relevance in chemotherapy resistance and DNA damage repair has also been addressed. However, little is known regarding the association between HOXB7 and chemotherapy resistance in esophageal squamous cell carcinoma (ESCC).
Methods
The association between HOXB7 expression detected by immunohistochemisty and tumor regression grade (TRG) and long‐term survival was analyzed in 143 ESCC patients who underwent neoadjuvant chemotherapy. CCK8 assay was used to examine the effect of cisplatin in a panel of four ESCC cell lines. A stable cell strain with HOXB7 knockdown of KYSE150 and KYSE450 was established to explore the effect on cisplatin sensitivity. The interaction of HOXB7 with Ku70, Ku80 and DNA‐PKcs was determined by GST‐pull down, coimmunoprecipitation and immunofluorescent colocalization. Finally, we investigated whether disrupting HOXB7 function by a synthetic peptide HXR9 blocking the formation of HOXB7/PBX could enhance cisplatin sensitivity in vitro and in vivo.
Results
High expression of HOXB7 was associated with cisplatin resistance and worse chemotherapy efficacy. HOXB7 knockdown reinforced cisplatin sensitivity. It was identified that HOXB7 interacts with Ku70, Ku80 and DNA‐PKcs. HOXB7 knockdown was related to the downregulation of Ku70, Ku80 and DNA‐PKcs as well as arrested cell cycle in S phase. HOXB7 inhibition by HXR9 had a synergistic effect to improve cisplatin sensitivity.
Conclusion
HOXB7 may be a biomarker for the prediction of chemoresistance of ESCC and serves as a promising therapeutic target.</description><subject>Antibodies</subject><subject>Antigens</subject><subject>Apoptosis</subject><subject>Cancer therapies</subject><subject>Cell cycle</subject><subject>Chemoresistance</subject><subject>Chemotherapy</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>DNA damage</subject><subject>DNA repair</subject><subject>Drug resistance</subject><subject>ESCC</subject><subject>Esophageal cancer</subject><subject>homeobox gene</subject><subject>Kinases</subject><subject>Life Sciences & Biomedicine</subject><subject>NHEJ</subject><subject>Oncology</subject><subject>Original</subject><subject>Respiratory System</subject><subject>Science & Technology</subject><subject>Squamous cell carcinoma</subject><subject>Tumors</subject><issn>1759-7706</issn><issn>1759-7714</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>WIN</sourceid><sourceid>AOWDO</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>DOA</sourceid><recordid>eNqNkk1v1DAQhiMEolXpmRuKxBFtaye2Y1-QlkA_pIpeisTNsp3JrldJnNrJov57ZrvLip5gLv565vWMX2fZe0ouKMYlrbhaVBVlF7SkrHiVnR53Xh_nRJxk5yltCEYpFSn42-ykpFxIwflpFm_uf36p8h4abyZIufNp7MzkhzxC8mkyg4McV5DCuDYrMF2eHmfThxlZ6Lrcmej8EHqTT-sY5tUa6W3ottDDMOWhzb9-X-aN6TEXJUfj47vsTWu6BOeH8Sz7cfXtob5Z3N1f39bLu4XjShWLUlhqDLSsKF1LVaWsLByX1FZSEmGFLEmlBJRWcgkMCldSIywIpSgRUEF5lt3udZtgNnqMvjfxSQfj9fNGiCtt4uRdB5o5oVxT2FYyyaBUBqAA7jhrLBW2Jaj1ea81zhbfymFv0XQvRF-eDH6tV2GrK0EEoRwFPh4EYnicIU16E-Y4YP-6YFxwVilKkbrcUy6GlCK0xxso0TvP9c5VvXNYP3uOGR_-LuzI_3EYgU974BfY0CbnAR09YvgpmFSswDIxdgXI_6drP-FPCUMd5mHCVH5I9R08_atw_VAv9x38BtLv2AU</recordid><startdate>202011</startdate><enddate>202011</enddate><creator>Zhou, Ting</creator><creator>Fu, Hao</creator><creator>Dong, Bin</creator><creator>Dai, Liang</creator><creator>Yang, Yongbo</creator><creator>Yan, Wanpu</creator><creator>Shen, Luyan</creator><general>John Wiley & Sons Australia, Ltd</general><general>Wiley</general><general>John Wiley & Sons, Inc</general><scope>24P</scope><scope>WIN</scope><scope>AOWDO</scope><scope>BLEPL</scope><scope>DTL</scope><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>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0003-4573-9872</orcidid></search><sort><creationdate>202011</creationdate><title>HOXB7 mediates cisplatin resistance in esophageal squamous cell carcinoma through involvement of DNA damage repair</title><author>Zhou, Ting ; Fu, Hao ; Dong, Bin ; Dai, Liang ; Yang, Yongbo ; Yan, Wanpu ; Shen, Luyan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5992-36b1aaef423cf1979b82c581b78806b6830796e3b858e4e2c31a6be699106e7e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Antibodies</topic><topic>Antigens</topic><topic>Apoptosis</topic><topic>Cancer therapies</topic><topic>Cell cycle</topic><topic>Chemoresistance</topic><topic>Chemotherapy</topic><topic>Deoxyribonucleic acid</topic><topic>DNA</topic><topic>DNA damage</topic><topic>DNA repair</topic><topic>Drug resistance</topic><topic>ESCC</topic><topic>Esophageal cancer</topic><topic>homeobox gene</topic><topic>Kinases</topic><topic>Life Sciences & Biomedicine</topic><topic>NHEJ</topic><topic>Oncology</topic><topic>Original</topic><topic>Respiratory System</topic><topic>Science & Technology</topic><topic>Squamous cell carcinoma</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhou, Ting</creatorcontrib><creatorcontrib>Fu, Hao</creatorcontrib><creatorcontrib>Dong, Bin</creatorcontrib><creatorcontrib>Dai, Liang</creatorcontrib><creatorcontrib>Yang, Yongbo</creatorcontrib><creatorcontrib>Yan, Wanpu</creatorcontrib><creatorcontrib>Shen, Luyan</creatorcontrib><collection>Wiley Online Library (Open Access Collection)</collection><collection>Wiley Online Library (Open Access Collection)</collection><collection>Web of Science - Science Citation Index Expanded - 2020</collection><collection>Web of Science Core Collection</collection><collection>Science Citation Index Expanded</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>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>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 Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Access via ProQuest (Open Access)</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>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Thoracic cancer</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhou, Ting</au><au>Fu, Hao</au><au>Dong, Bin</au><au>Dai, Liang</au><au>Yang, Yongbo</au><au>Yan, Wanpu</au><au>Shen, Luyan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>HOXB7 mediates cisplatin resistance in esophageal squamous cell carcinoma through involvement of DNA damage repair</atitle><jtitle>Thoracic cancer</jtitle><stitle>THORAC CANCER</stitle><addtitle>Thorac Cancer</addtitle><date>2020-11</date><risdate>2020</risdate><volume>11</volume><issue>11</issue><spage>3071</spage><epage>3085</epage><pages>3071-3085</pages><issn>1759-7706</issn><eissn>1759-7714</eissn><abstract>Background
DNA damage repair is an important mechanism of platinum resistance. HOXB7 is one member of HOX family genes, which are essential developmental regulators and frequently dysregulated in cancer. Recently, its relevance in chemotherapy resistance and DNA damage repair has also been addressed. However, little is known regarding the association between HOXB7 and chemotherapy resistance in esophageal squamous cell carcinoma (ESCC).
Methods
The association between HOXB7 expression detected by immunohistochemisty and tumor regression grade (TRG) and long‐term survival was analyzed in 143 ESCC patients who underwent neoadjuvant chemotherapy. CCK8 assay was used to examine the effect of cisplatin in a panel of four ESCC cell lines. A stable cell strain with HOXB7 knockdown of KYSE150 and KYSE450 was established to explore the effect on cisplatin sensitivity. The interaction of HOXB7 with Ku70, Ku80 and DNA‐PKcs was determined by GST‐pull down, coimmunoprecipitation and immunofluorescent colocalization. Finally, we investigated whether disrupting HOXB7 function by a synthetic peptide HXR9 blocking the formation of HOXB7/PBX could enhance cisplatin sensitivity in vitro and in vivo.
Results
High expression of HOXB7 was associated with cisplatin resistance and worse chemotherapy efficacy. HOXB7 knockdown reinforced cisplatin sensitivity. It was identified that HOXB7 interacts with Ku70, Ku80 and DNA‐PKcs. HOXB7 knockdown was related to the downregulation of Ku70, Ku80 and DNA‐PKcs as well as arrested cell cycle in S phase. HOXB7 inhibition by HXR9 had a synergistic effect to improve cisplatin sensitivity.
Conclusion
HOXB7 may be a biomarker for the prediction of chemoresistance of ESCC and serves as a promising therapeutic target.</abstract><cop>Melbourne</cop><pub>John Wiley & Sons Australia, Ltd</pub><pmid>31568655</pmid><doi>10.1111/1759-7714.13142</doi><tpages>15</tpages><orcidid>https://orcid.org/0000-0003-4573-9872</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Antibodies Antigens Apoptosis Cancer therapies Cell cycle Chemoresistance Chemotherapy Deoxyribonucleic acid DNA DNA damage DNA repair Drug resistance ESCC Esophageal cancer homeobox gene Kinases Life Sciences & Biomedicine NHEJ Oncology Original Respiratory System Science & Technology Squamous cell carcinoma Tumors |
| title | HOXB7 mediates cisplatin resistance in esophageal squamous cell carcinoma through involvement of DNA damage repair |
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