Forkhead box D1 promotes EMT and chemoresistance by upregulating lncRNA CYTOR in oral squamous cell carcinoma
Chemotherapy regimens containing cisplatin remain the first-line treatments for patients with oral squamous cell cancer (OSCC); however, the treatment effect is often transient because of chemoresistance and recurrence. Understanding the mechanisms of chemoresistance in OSCC might provide novel targ...
Gespeichert in:
| Veröffentlicht in: | Cancer letters 2021-04, Vol.503, p.43-53 |
|---|---|
| Hauptverfasser: | , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 53 |
|---|---|
| container_issue | |
| container_start_page | 43 |
| container_title | Cancer letters |
| container_volume | 503 |
| creator | Chen, Shuwei Yang, Muwen Wang, Chunyang Ouyang, Ying Chen, Xiangfu Bai, Jiewen Hu, Yameng Song, Ming Zhang, Siyi Zhang, Quan |
| description | Chemotherapy regimens containing cisplatin remain the first-line treatments for patients with oral squamous cell cancer (OSCC); however, the treatment effect is often transient because of chemoresistance and recurrence. Understanding the mechanisms of chemoresistance in OSCC might provide novel targetable vulnerabilities. In the present study, we revealed that Forkhead box D1 (FOXD1) is upregulated in OSCC and predicted poor prognosis. Moreover, ectopic expression of FOXD1 promoted, while silencing of FOXD1 inhibited, the epithelial-mesenchymal transition (EMT) and chemoresistance of OSCC, both in vitro and in vivo. Mechanistically, FOXD1 binds to the promoter of long non-coding RNA Cytoskeleton Regulator RNA (CYTOR) and activates its transcription. CYTOR then acts as a competing endogenous RNA to inhibit miR-1252–5p and miR-3148, thus upregulating lipoma preferred partner (LPP) expression. Importantly, the CYTOR/LPP axis was proven to be essential for FOXD1-induced EMT and chemoresistance in OSCC. These findings reveal a novel mechanism for the chemotherapy resistance of OSCC, suggesting that FOXD1 might be a potential prognostic marker and anti-resistance therapeutic target.
•Forkhead box D1 (FOXD1) is upregulated in OSCC and predicted poor prognosis.•FOXD1 promotes the epithelial-mesenchymal transition and chemoresistance of OSCC.•FOXD1 binds to and activates the transcription of lncRNA CYTOR.•CYTOR acts as a ceRNA for miR-1252-5p and miR-3148 to upregulate LPP expression.•The CYTOR/LPP axis is essential for FOXD1-induced chemoresistance of OSCC. |
| doi_str_mv | 10.1016/j.canlet.2020.11.046 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2473404525</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0304383520306443</els_id><sourcerecordid>2501855345</sourcerecordid><originalsourceid>FETCH-LOGICAL-c502t-cb201d428144c44b470e3b42944f5efd731367c2efe3d38007a731f621d845883</originalsourceid><addsrcrecordid>eNp9kU1vEzEQhi0EoqHwDxCyxIXLBn-Ms-4FqUq_kAqVqnDgZHnt2dZh107tXUT_PY5SOHDgNNLomZl33peQt5wtOeOrj9uls3HAaSmYqC2-ZLB6RhZct6JpTzR7ThZMMmikluqIvCplyxhT0KqX5EhKqYQAvSDjRco_7tF62qVf9IzTXU5jmrDQ8y8baqOn7h7HlLGEMtnokHaPdN5lvJsHO4V4R4fobr-e0vX3zc0tDZGmbAdaHmY7prlQh8NAnc0uxDTa1-RFb4eCb57qMfl2cb5ZXzXXN5ef16fXjVNMTI3rBOMehOYADqCDlqHsQJwA9Ap730ouV60T2KP0UjPW2trqV4J7DUpreUw-HPbWbx5mLJMZQ9lLsRGrKiOglcBACVXR9_-g2zTnWNUZoRjXSknYU3CgXE6lZOzNLofR5kfDmdnHYbbmEIfZx2E4NzWOOvbuafncjej_Dv3xvwKfDgBWN34GzKa4gNVmHzK6yfgU_n_hNxrXm2A</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2501855345</pqid></control><display><type>article</type><title>Forkhead box D1 promotes EMT and chemoresistance by upregulating lncRNA CYTOR in oral squamous cell carcinoma</title><source>MEDLINE</source><source>Access via ScienceDirect (Elsevier)</source><creator>Chen, Shuwei ; Yang, Muwen ; Wang, Chunyang ; Ouyang, Ying ; Chen, Xiangfu ; Bai, Jiewen ; Hu, Yameng ; Song, Ming ; Zhang, Siyi ; Zhang, Quan</creator><creatorcontrib>Chen, Shuwei ; Yang, Muwen ; Wang, Chunyang ; Ouyang, Ying ; Chen, Xiangfu ; Bai, Jiewen ; Hu, Yameng ; Song, Ming ; Zhang, Siyi ; Zhang, Quan</creatorcontrib><description>Chemotherapy regimens containing cisplatin remain the first-line treatments for patients with oral squamous cell cancer (OSCC); however, the treatment effect is often transient because of chemoresistance and recurrence. Understanding the mechanisms of chemoresistance in OSCC might provide novel targetable vulnerabilities. In the present study, we revealed that Forkhead box D1 (FOXD1) is upregulated in OSCC and predicted poor prognosis. Moreover, ectopic expression of FOXD1 promoted, while silencing of FOXD1 inhibited, the epithelial-mesenchymal transition (EMT) and chemoresistance of OSCC, both in vitro and in vivo. Mechanistically, FOXD1 binds to the promoter of long non-coding RNA Cytoskeleton Regulator RNA (CYTOR) and activates its transcription. CYTOR then acts as a competing endogenous RNA to inhibit miR-1252–5p and miR-3148, thus upregulating lipoma preferred partner (LPP) expression. Importantly, the CYTOR/LPP axis was proven to be essential for FOXD1-induced EMT and chemoresistance in OSCC. These findings reveal a novel mechanism for the chemotherapy resistance of OSCC, suggesting that FOXD1 might be a potential prognostic marker and anti-resistance therapeutic target.
•Forkhead box D1 (FOXD1) is upregulated in OSCC and predicted poor prognosis.•FOXD1 promotes the epithelial-mesenchymal transition and chemoresistance of OSCC.•FOXD1 binds to and activates the transcription of lncRNA CYTOR.•CYTOR acts as a ceRNA for miR-1252-5p and miR-3148 to upregulate LPP expression.•The CYTOR/LPP axis is essential for FOXD1-induced chemoresistance of OSCC.</description><identifier>ISSN: 0304-3835</identifier><identifier>EISSN: 1872-7980</identifier><identifier>DOI: 10.1016/j.canlet.2020.11.046</identifier><identifier>PMID: 33352248</identifier><language>eng</language><publisher>Ireland: Elsevier B.V</publisher><subject>Animals ; Antibodies ; Binding sites ; Breast cancer ; Carcinoma, Squamous Cell - genetics ; Carcinoma, Squamous Cell - metabolism ; Carcinoma, Squamous Cell - pathology ; Cell Line, Tumor ; Cervical cancer ; Chemoresistance ; Chemotherapy ; Cisplatin ; CYTOR ; Cytoskeletal Proteins - genetics ; Cytoskeleton ; Deoxyribonucleic acid ; DNA ; Drug Resistance, Neoplasm ; Ectopic expression ; EMT ; Epithelial-Mesenchymal Transition ; Forkhead protein ; Forkhead Transcription Factors - genetics ; Forkhead Transcription Factors - metabolism ; FOXD1 ; Gene expression ; Gene Expression Regulation, Neoplastic ; Genotype & phenotype ; Humans ; LIM Domain Proteins - genetics ; Lipoma ; Medical prognosis ; Mesenchyme ; Metastasis ; Mice ; MicroRNAs - genetics ; Mouth Neoplasms - genetics ; Mouth Neoplasms - metabolism ; Mouth Neoplasms - pathology ; Neoplasm Transplantation ; Non-coding RNA ; Oral cancer ; Oral squamous cell carcinoma ; OSCC ; Prognosis ; Promoter Regions, Genetic ; Proteins ; RNA polymerase ; RNA, Long Noncoding - genetics ; Signal transduction ; Squamous cell carcinoma ; Transcription ; Up-Regulation</subject><ispartof>Cancer letters, 2021-04, Vol.503, p.43-53</ispartof><rights>2020 The Authors</rights><rights>Copyright © 2020 The Authors. Published by Elsevier B.V. All rights reserved.</rights><rights>2020. The Authors</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c502t-cb201d428144c44b470e3b42944f5efd731367c2efe3d38007a731f621d845883</citedby><cites>FETCH-LOGICAL-c502t-cb201d428144c44b470e3b42944f5efd731367c2efe3d38007a731f621d845883</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.canlet.2020.11.046$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33352248$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chen, Shuwei</creatorcontrib><creatorcontrib>Yang, Muwen</creatorcontrib><creatorcontrib>Wang, Chunyang</creatorcontrib><creatorcontrib>Ouyang, Ying</creatorcontrib><creatorcontrib>Chen, Xiangfu</creatorcontrib><creatorcontrib>Bai, Jiewen</creatorcontrib><creatorcontrib>Hu, Yameng</creatorcontrib><creatorcontrib>Song, Ming</creatorcontrib><creatorcontrib>Zhang, Siyi</creatorcontrib><creatorcontrib>Zhang, Quan</creatorcontrib><title>Forkhead box D1 promotes EMT and chemoresistance by upregulating lncRNA CYTOR in oral squamous cell carcinoma</title><title>Cancer letters</title><addtitle>Cancer Lett</addtitle><description>Chemotherapy regimens containing cisplatin remain the first-line treatments for patients with oral squamous cell cancer (OSCC); however, the treatment effect is often transient because of chemoresistance and recurrence. Understanding the mechanisms of chemoresistance in OSCC might provide novel targetable vulnerabilities. In the present study, we revealed that Forkhead box D1 (FOXD1) is upregulated in OSCC and predicted poor prognosis. Moreover, ectopic expression of FOXD1 promoted, while silencing of FOXD1 inhibited, the epithelial-mesenchymal transition (EMT) and chemoresistance of OSCC, both in vitro and in vivo. Mechanistically, FOXD1 binds to the promoter of long non-coding RNA Cytoskeleton Regulator RNA (CYTOR) and activates its transcription. CYTOR then acts as a competing endogenous RNA to inhibit miR-1252–5p and miR-3148, thus upregulating lipoma preferred partner (LPP) expression. Importantly, the CYTOR/LPP axis was proven to be essential for FOXD1-induced EMT and chemoresistance in OSCC. These findings reveal a novel mechanism for the chemotherapy resistance of OSCC, suggesting that FOXD1 might be a potential prognostic marker and anti-resistance therapeutic target.
•Forkhead box D1 (FOXD1) is upregulated in OSCC and predicted poor prognosis.•FOXD1 promotes the epithelial-mesenchymal transition and chemoresistance of OSCC.•FOXD1 binds to and activates the transcription of lncRNA CYTOR.•CYTOR acts as a ceRNA for miR-1252-5p and miR-3148 to upregulate LPP expression.•The CYTOR/LPP axis is essential for FOXD1-induced chemoresistance of OSCC.</description><subject>Animals</subject><subject>Antibodies</subject><subject>Binding sites</subject><subject>Breast cancer</subject><subject>Carcinoma, Squamous Cell - genetics</subject><subject>Carcinoma, Squamous Cell - metabolism</subject><subject>Carcinoma, Squamous Cell - pathology</subject><subject>Cell Line, Tumor</subject><subject>Cervical cancer</subject><subject>Chemoresistance</subject><subject>Chemotherapy</subject><subject>Cisplatin</subject><subject>CYTOR</subject><subject>Cytoskeletal Proteins - genetics</subject><subject>Cytoskeleton</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>Drug Resistance, Neoplasm</subject><subject>Ectopic expression</subject><subject>EMT</subject><subject>Epithelial-Mesenchymal Transition</subject><subject>Forkhead protein</subject><subject>Forkhead Transcription Factors - genetics</subject><subject>Forkhead Transcription Factors - metabolism</subject><subject>FOXD1</subject><subject>Gene expression</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Genotype & phenotype</subject><subject>Humans</subject><subject>LIM Domain Proteins - genetics</subject><subject>Lipoma</subject><subject>Medical prognosis</subject><subject>Mesenchyme</subject><subject>Metastasis</subject><subject>Mice</subject><subject>MicroRNAs - genetics</subject><subject>Mouth Neoplasms - genetics</subject><subject>Mouth Neoplasms - metabolism</subject><subject>Mouth Neoplasms - pathology</subject><subject>Neoplasm Transplantation</subject><subject>Non-coding RNA</subject><subject>Oral cancer</subject><subject>Oral squamous cell carcinoma</subject><subject>OSCC</subject><subject>Prognosis</subject><subject>Promoter Regions, Genetic</subject><subject>Proteins</subject><subject>RNA polymerase</subject><subject>RNA, Long Noncoding - genetics</subject><subject>Signal transduction</subject><subject>Squamous cell carcinoma</subject><subject>Transcription</subject><subject>Up-Regulation</subject><issn>0304-3835</issn><issn>1872-7980</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kU1vEzEQhi0EoqHwDxCyxIXLBn-Ms-4FqUq_kAqVqnDgZHnt2dZh107tXUT_PY5SOHDgNNLomZl33peQt5wtOeOrj9uls3HAaSmYqC2-ZLB6RhZct6JpTzR7ThZMMmikluqIvCplyxhT0KqX5EhKqYQAvSDjRco_7tF62qVf9IzTXU5jmrDQ8y8baqOn7h7HlLGEMtnokHaPdN5lvJsHO4V4R4fobr-e0vX3zc0tDZGmbAdaHmY7prlQh8NAnc0uxDTa1-RFb4eCb57qMfl2cb5ZXzXXN5ef16fXjVNMTI3rBOMehOYADqCDlqHsQJwA9Ap730ouV60T2KP0UjPW2trqV4J7DUpreUw-HPbWbx5mLJMZQ9lLsRGrKiOglcBACVXR9_-g2zTnWNUZoRjXSknYU3CgXE6lZOzNLofR5kfDmdnHYbbmEIfZx2E4NzWOOvbuafncjej_Dv3xvwKfDgBWN34GzKa4gNVmHzK6yfgU_n_hNxrXm2A</recordid><startdate>20210410</startdate><enddate>20210410</enddate><creator>Chen, Shuwei</creator><creator>Yang, Muwen</creator><creator>Wang, Chunyang</creator><creator>Ouyang, Ying</creator><creator>Chen, Xiangfu</creator><creator>Bai, Jiewen</creator><creator>Hu, Yameng</creator><creator>Song, Ming</creator><creator>Zhang, Siyi</creator><creator>Zhang, Quan</creator><general>Elsevier B.V</general><general>Elsevier Limited</general><scope>6I.</scope><scope>AAFTH</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>7TO</scope><scope>7U9</scope><scope>H94</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>7X8</scope></search><sort><creationdate>20210410</creationdate><title>Forkhead box D1 promotes EMT and chemoresistance by upregulating lncRNA CYTOR in oral squamous cell carcinoma</title><author>Chen, Shuwei ; Yang, Muwen ; Wang, Chunyang ; Ouyang, Ying ; Chen, Xiangfu ; Bai, Jiewen ; Hu, Yameng ; Song, Ming ; Zhang, Siyi ; Zhang, Quan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c502t-cb201d428144c44b470e3b42944f5efd731367c2efe3d38007a731f621d845883</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Animals</topic><topic>Antibodies</topic><topic>Binding sites</topic><topic>Breast cancer</topic><topic>Carcinoma, Squamous Cell - genetics</topic><topic>Carcinoma, Squamous Cell - metabolism</topic><topic>Carcinoma, Squamous Cell - pathology</topic><topic>Cell Line, Tumor</topic><topic>Cervical cancer</topic><topic>Chemoresistance</topic><topic>Chemotherapy</topic><topic>Cisplatin</topic><topic>CYTOR</topic><topic>Cytoskeletal Proteins - genetics</topic><topic>Cytoskeleton</topic><topic>Deoxyribonucleic acid</topic><topic>DNA</topic><topic>Drug Resistance, Neoplasm</topic><topic>Ectopic expression</topic><topic>EMT</topic><topic>Epithelial-Mesenchymal Transition</topic><topic>Forkhead protein</topic><topic>Forkhead Transcription Factors - genetics</topic><topic>Forkhead Transcription Factors - metabolism</topic><topic>FOXD1</topic><topic>Gene expression</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Genotype & phenotype</topic><topic>Humans</topic><topic>LIM Domain Proteins - genetics</topic><topic>Lipoma</topic><topic>Medical prognosis</topic><topic>Mesenchyme</topic><topic>Metastasis</topic><topic>Mice</topic><topic>MicroRNAs - genetics</topic><topic>Mouth Neoplasms - genetics</topic><topic>Mouth Neoplasms - metabolism</topic><topic>Mouth Neoplasms - pathology</topic><topic>Neoplasm Transplantation</topic><topic>Non-coding RNA</topic><topic>Oral cancer</topic><topic>Oral squamous cell carcinoma</topic><topic>OSCC</topic><topic>Prognosis</topic><topic>Promoter Regions, Genetic</topic><topic>Proteins</topic><topic>RNA polymerase</topic><topic>RNA, Long Noncoding - genetics</topic><topic>Signal transduction</topic><topic>Squamous cell carcinoma</topic><topic>Transcription</topic><topic>Up-Regulation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chen, Shuwei</creatorcontrib><creatorcontrib>Yang, Muwen</creatorcontrib><creatorcontrib>Wang, Chunyang</creatorcontrib><creatorcontrib>Ouyang, Ying</creatorcontrib><creatorcontrib>Chen, Xiangfu</creatorcontrib><creatorcontrib>Bai, Jiewen</creatorcontrib><creatorcontrib>Hu, Yameng</creatorcontrib><creatorcontrib>Song, Ming</creatorcontrib><creatorcontrib>Zhang, Siyi</creatorcontrib><creatorcontrib>Zhang, Quan</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><jtitle>Cancer letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chen, Shuwei</au><au>Yang, Muwen</au><au>Wang, Chunyang</au><au>Ouyang, Ying</au><au>Chen, Xiangfu</au><au>Bai, Jiewen</au><au>Hu, Yameng</au><au>Song, Ming</au><au>Zhang, Siyi</au><au>Zhang, Quan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Forkhead box D1 promotes EMT and chemoresistance by upregulating lncRNA CYTOR in oral squamous cell carcinoma</atitle><jtitle>Cancer letters</jtitle><addtitle>Cancer Lett</addtitle><date>2021-04-10</date><risdate>2021</risdate><volume>503</volume><spage>43</spage><epage>53</epage><pages>43-53</pages><issn>0304-3835</issn><eissn>1872-7980</eissn><abstract>Chemotherapy regimens containing cisplatin remain the first-line treatments for patients with oral squamous cell cancer (OSCC); however, the treatment effect is often transient because of chemoresistance and recurrence. Understanding the mechanisms of chemoresistance in OSCC might provide novel targetable vulnerabilities. In the present study, we revealed that Forkhead box D1 (FOXD1) is upregulated in OSCC and predicted poor prognosis. Moreover, ectopic expression of FOXD1 promoted, while silencing of FOXD1 inhibited, the epithelial-mesenchymal transition (EMT) and chemoresistance of OSCC, both in vitro and in vivo. Mechanistically, FOXD1 binds to the promoter of long non-coding RNA Cytoskeleton Regulator RNA (CYTOR) and activates its transcription. CYTOR then acts as a competing endogenous RNA to inhibit miR-1252–5p and miR-3148, thus upregulating lipoma preferred partner (LPP) expression. Importantly, the CYTOR/LPP axis was proven to be essential for FOXD1-induced EMT and chemoresistance in OSCC. These findings reveal a novel mechanism for the chemotherapy resistance of OSCC, suggesting that FOXD1 might be a potential prognostic marker and anti-resistance therapeutic target.
•Forkhead box D1 (FOXD1) is upregulated in OSCC and predicted poor prognosis.•FOXD1 promotes the epithelial-mesenchymal transition and chemoresistance of OSCC.•FOXD1 binds to and activates the transcription of lncRNA CYTOR.•CYTOR acts as a ceRNA for miR-1252-5p and miR-3148 to upregulate LPP expression.•The CYTOR/LPP axis is essential for FOXD1-induced chemoresistance of OSCC.</abstract><cop>Ireland</cop><pub>Elsevier B.V</pub><pmid>33352248</pmid><doi>10.1016/j.canlet.2020.11.046</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0304-3835 |
| ispartof | Cancer letters, 2021-04, Vol.503, p.43-53 |
| issn | 0304-3835 1872-7980 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_2473404525 |
| source | MEDLINE; Access via ScienceDirect (Elsevier) |
| subjects | Animals Antibodies Binding sites Breast cancer Carcinoma, Squamous Cell - genetics Carcinoma, Squamous Cell - metabolism Carcinoma, Squamous Cell - pathology Cell Line, Tumor Cervical cancer Chemoresistance Chemotherapy Cisplatin CYTOR Cytoskeletal Proteins - genetics Cytoskeleton Deoxyribonucleic acid DNA Drug Resistance, Neoplasm Ectopic expression EMT Epithelial-Mesenchymal Transition Forkhead protein Forkhead Transcription Factors - genetics Forkhead Transcription Factors - metabolism FOXD1 Gene expression Gene Expression Regulation, Neoplastic Genotype & phenotype Humans LIM Domain Proteins - genetics Lipoma Medical prognosis Mesenchyme Metastasis Mice MicroRNAs - genetics Mouth Neoplasms - genetics Mouth Neoplasms - metabolism Mouth Neoplasms - pathology Neoplasm Transplantation Non-coding RNA Oral cancer Oral squamous cell carcinoma OSCC Prognosis Promoter Regions, Genetic Proteins RNA polymerase RNA, Long Noncoding - genetics Signal transduction Squamous cell carcinoma Transcription Up-Regulation |
| title | Forkhead box D1 promotes EMT and chemoresistance by upregulating lncRNA CYTOR in oral squamous cell carcinoma |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-22T05%3A12%3A08IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Forkhead%20box%20D1%20promotes%20EMT%20and%20chemoresistance%20by%20upregulating%20lncRNA%20CYTOR%20in%20oral%20squamous%20cell%20carcinoma&rft.jtitle=Cancer%20letters&rft.au=Chen,%20Shuwei&rft.date=2021-04-10&rft.volume=503&rft.spage=43&rft.epage=53&rft.pages=43-53&rft.issn=0304-3835&rft.eissn=1872-7980&rft_id=info:doi/10.1016/j.canlet.2020.11.046&rft_dat=%3Cproquest_cross%3E2501855345%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2501855345&rft_id=info:pmid/33352248&rft_els_id=S0304383520306443&rfr_iscdi=true |