TGF- β downregulation overcomes gemcitabine resistance in oral squamous cell carcinoma
OBJECTIVE: The aim of this study was to explore the mechanisms by which oral cancer acquires resistance to gemcitabine. METHODS: Oral squamous cell carcinoma (OSCC) cells were treated with gemcitabine upon infection or with a lentivirus harboring short hairpin RNA (shRNA) targeted to transforming gr...
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| Veröffentlicht in: | Cancer biomarkers : section A of Disease markers 2020-01, Vol.29 (2), p.179-187 |
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| creator | Xuan, Yun-Ze Jin, Cheng-Ri Yang, Kang-Juan |
| description | OBJECTIVE:
The aim of this study was to explore the mechanisms by which oral cancer acquires resistance to gemcitabine.
METHODS:
Oral squamous cell carcinoma (OSCC) cells were treated with gemcitabine upon infection or with a lentivirus harboring short hairpin RNA (shRNA) targeted to transforming growth factor-
β
(TGF-
β
). Then, Western blot, ELISA, migration assay, MTT assay, and animal experiments were used to explore the mechanism of resistance to gemcitabine treatment.
RESULTS:
After the treatment of non-transfected cells with gemcitabine, NF-
κ
B and AKT activities were increased, which may have induced the OSCC resistance to gemcitabine. Then, we found that TGF-
β
downregulation effectively reduced NF-
κ
B and AKT phosphorylation levels after the administration of gemcitabine and increased the OSCC sensitivity to gemcitabine, resulting in cell death and the blunting of OSCC resistance to gemcitabine. The EMT was also reduced by TGF-
β
downregulation combined with gemcitabine treatment.
CONCLUSION:
Cellular levels of TGF-
β
constitute an important factor in gemcitabine resistance and TGF-
β
silencing might represent a novel and potent strategy for overcoming OSCC resistance to gemcitabine. |
| doi_str_mv | 10.3233/CBM-201456 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_AFRWT</sourceid><recordid>TN_cdi_proquest_miscellaneous_2430093975</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sage_id>10.3233_CBM-201456</sage_id><sourcerecordid>2430093975</sourcerecordid><originalsourceid>FETCH-LOGICAL-c324t-7ac5eb5fd5c3df5388b27b60b5532d1030bc541c30ef758391e6a22b736a56d83</originalsourceid><addsrcrecordid>eNpt0MFKxDAUBdAgCo6jG78g4EIRqkle0rRLHZxRUNyMuCxpmg4Z2mYmaRV_yw_xm8xQQRBX7y0Ol8tF6JSSK2AA17Pbp4QRykW6hyY0kyLJRM724y8kTwgVcIiOQlgTwoGyfIJel4t5gr8-ceXeO29WQ6N66zrs3ozXrjUBr0yrba9K2xnsTbChV5022EbjVYPDdlCtGwLWpmmwVl7bzrXqGB3Uqgnm5OdO0cv8bjm7Tx6fFw-zm8dEA-N9IpUWphR1JTRUtYAsK5ksU1IKAayiBEipBacaiKmlyCCnJlWMlRJSJdIqgym6GHM33m0HE_qitWFXRXUmtioYB0JyyKWI9OwPXbvBd7FdVIJISTlnUV2OSnsXgjd1sfG2Vf6joKTYbVzEjYtx44jPRxzUyvzG_SO_AYdkepo</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2450771442</pqid></control><display><type>article</type><title>TGF- β downregulation overcomes gemcitabine resistance in oral squamous cell carcinoma</title><source>Sage Journals GOLD Open Access 2024</source><creator>Xuan, Yun-Ze ; Jin, Cheng-Ri ; Yang, Kang-Juan</creator><creatorcontrib>Xuan, Yun-Ze ; Jin, Cheng-Ri ; Yang, Kang-Juan</creatorcontrib><description>OBJECTIVE:
The aim of this study was to explore the mechanisms by which oral cancer acquires resistance to gemcitabine.
METHODS:
Oral squamous cell carcinoma (OSCC) cells were treated with gemcitabine upon infection or with a lentivirus harboring short hairpin RNA (shRNA) targeted to transforming growth factor-
β
(TGF-
β
). Then, Western blot, ELISA, migration assay, MTT assay, and animal experiments were used to explore the mechanism of resistance to gemcitabine treatment.
RESULTS:
After the treatment of non-transfected cells with gemcitabine, NF-
κ
B and AKT activities were increased, which may have induced the OSCC resistance to gemcitabine. Then, we found that TGF-
β
downregulation effectively reduced NF-
κ
B and AKT phosphorylation levels after the administration of gemcitabine and increased the OSCC sensitivity to gemcitabine, resulting in cell death and the blunting of OSCC resistance to gemcitabine. The EMT was also reduced by TGF-
β
downregulation combined with gemcitabine treatment.
CONCLUSION:
Cellular levels of TGF-
β
constitute an important factor in gemcitabine resistance and TGF-
β
silencing might represent a novel and potent strategy for overcoming OSCC resistance to gemcitabine.</description><identifier>ISSN: 1574-0153</identifier><identifier>EISSN: 1875-8592</identifier><identifier>DOI: 10.3233/CBM-201456</identifier><language>eng</language><publisher>London, England: SAGE Publications</publisher><subject>AKT protein ; Animal research ; Cancer ; Cell death ; Enzyme-linked immunosorbent assay ; Gemcitabine ; Growth factors ; Oral cancer ; Oral squamous cell carcinoma ; Phosphorylation ; Resistance factors ; Ribonucleic acid ; RNA ; Squamous cell carcinoma ; Transforming growth factor-b</subject><ispartof>Cancer biomarkers : section A of Disease markers, 2020-01, Vol.29 (2), p.179-187</ispartof><rights>2020 – IOS Press and the authors. All rights reserved</rights><rights>Copyright IOS Press BV 2020</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c324t-7ac5eb5fd5c3df5388b27b60b5532d1030bc541c30ef758391e6a22b736a56d83</citedby><cites>FETCH-LOGICAL-c324t-7ac5eb5fd5c3df5388b27b60b5532d1030bc541c30ef758391e6a22b736a56d83</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://journals.sagepub.com/doi/pdf/10.3233/CBM-201456$$EPDF$$P50$$Gsage$$H</linktopdf><linktohtml>$$Uhttps://journals.sagepub.com/doi/10.3233/CBM-201456$$EHTML$$P50$$Gsage$$H</linktohtml><link.rule.ids>314,777,781,21947,27834,27905,27906,44926,45314</link.rule.ids><linktorsrc>$$Uhttps://journals.sagepub.com/doi/full/10.3233/CBM-201456?utm_source=summon&utm_medium=discovery-provider$$EView_record_in_SAGE_Publications$$FView_record_in_$$GSAGE_Publications</linktorsrc></links><search><creatorcontrib>Xuan, Yun-Ze</creatorcontrib><creatorcontrib>Jin, Cheng-Ri</creatorcontrib><creatorcontrib>Yang, Kang-Juan</creatorcontrib><title>TGF- β downregulation overcomes gemcitabine resistance in oral squamous cell carcinoma</title><title>Cancer biomarkers : section A of Disease markers</title><description>OBJECTIVE:
The aim of this study was to explore the mechanisms by which oral cancer acquires resistance to gemcitabine.
METHODS:
Oral squamous cell carcinoma (OSCC) cells were treated with gemcitabine upon infection or with a lentivirus harboring short hairpin RNA (shRNA) targeted to transforming growth factor-
β
(TGF-
β
). Then, Western blot, ELISA, migration assay, MTT assay, and animal experiments were used to explore the mechanism of resistance to gemcitabine treatment.
RESULTS:
After the treatment of non-transfected cells with gemcitabine, NF-
κ
B and AKT activities were increased, which may have induced the OSCC resistance to gemcitabine. Then, we found that TGF-
β
downregulation effectively reduced NF-
κ
B and AKT phosphorylation levels after the administration of gemcitabine and increased the OSCC sensitivity to gemcitabine, resulting in cell death and the blunting of OSCC resistance to gemcitabine. The EMT was also reduced by TGF-
β
downregulation combined with gemcitabine treatment.
CONCLUSION:
Cellular levels of TGF-
β
constitute an important factor in gemcitabine resistance and TGF-
β
silencing might represent a novel and potent strategy for overcoming OSCC resistance to gemcitabine.</description><subject>AKT protein</subject><subject>Animal research</subject><subject>Cancer</subject><subject>Cell death</subject><subject>Enzyme-linked immunosorbent assay</subject><subject>Gemcitabine</subject><subject>Growth factors</subject><subject>Oral cancer</subject><subject>Oral squamous cell carcinoma</subject><subject>Phosphorylation</subject><subject>Resistance factors</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>Squamous cell carcinoma</subject><subject>Transforming growth factor-b</subject><issn>1574-0153</issn><issn>1875-8592</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><recordid>eNpt0MFKxDAUBdAgCo6jG78g4EIRqkle0rRLHZxRUNyMuCxpmg4Z2mYmaRV_yw_xm8xQQRBX7y0Ol8tF6JSSK2AA17Pbp4QRykW6hyY0kyLJRM724y8kTwgVcIiOQlgTwoGyfIJel4t5gr8-ceXeO29WQ6N66zrs3ozXrjUBr0yrba9K2xnsTbChV5022EbjVYPDdlCtGwLWpmmwVl7bzrXqGB3Uqgnm5OdO0cv8bjm7Tx6fFw-zm8dEA-N9IpUWphR1JTRUtYAsK5ksU1IKAayiBEipBacaiKmlyCCnJlWMlRJSJdIqgym6GHM33m0HE_qitWFXRXUmtioYB0JyyKWI9OwPXbvBd7FdVIJISTlnUV2OSnsXgjd1sfG2Vf6joKTYbVzEjYtx44jPRxzUyvzG_SO_AYdkepo</recordid><startdate>20200101</startdate><enddate>20200101</enddate><creator>Xuan, Yun-Ze</creator><creator>Jin, Cheng-Ri</creator><creator>Yang, Kang-Juan</creator><general>SAGE Publications</general><general>IOS Press BV</general><scope>AAYXX</scope><scope>CITATION</scope><scope>7TM</scope><scope>7TO</scope><scope>7U7</scope><scope>C1K</scope><scope>H94</scope><scope>K9.</scope><scope>7X8</scope></search><sort><creationdate>20200101</creationdate><title>TGF- β downregulation overcomes gemcitabine resistance in oral squamous cell carcinoma</title><author>Xuan, Yun-Ze ; Jin, Cheng-Ri ; Yang, Kang-Juan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c324t-7ac5eb5fd5c3df5388b27b60b5532d1030bc541c30ef758391e6a22b736a56d83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>AKT protein</topic><topic>Animal research</topic><topic>Cancer</topic><topic>Cell death</topic><topic>Enzyme-linked immunosorbent assay</topic><topic>Gemcitabine</topic><topic>Growth factors</topic><topic>Oral cancer</topic><topic>Oral squamous cell carcinoma</topic><topic>Phosphorylation</topic><topic>Resistance factors</topic><topic>Ribonucleic acid</topic><topic>RNA</topic><topic>Squamous cell carcinoma</topic><topic>Transforming growth factor-b</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Xuan, Yun-Ze</creatorcontrib><creatorcontrib>Jin, Cheng-Ri</creatorcontrib><creatorcontrib>Yang, Kang-Juan</creatorcontrib><collection>CrossRef</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>Cancer biomarkers : section A of Disease markers</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext_linktorsrc</fulltext></delivery><addata><au>Xuan, Yun-Ze</au><au>Jin, Cheng-Ri</au><au>Yang, Kang-Juan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>TGF- β downregulation overcomes gemcitabine resistance in oral squamous cell carcinoma</atitle><jtitle>Cancer biomarkers : section A of Disease markers</jtitle><date>2020-01-01</date><risdate>2020</risdate><volume>29</volume><issue>2</issue><spage>179</spage><epage>187</epage><pages>179-187</pages><issn>1574-0153</issn><eissn>1875-8592</eissn><abstract>OBJECTIVE:
The aim of this study was to explore the mechanisms by which oral cancer acquires resistance to gemcitabine.
METHODS:
Oral squamous cell carcinoma (OSCC) cells were treated with gemcitabine upon infection or with a lentivirus harboring short hairpin RNA (shRNA) targeted to transforming growth factor-
β
(TGF-
β
). Then, Western blot, ELISA, migration assay, MTT assay, and animal experiments were used to explore the mechanism of resistance to gemcitabine treatment.
RESULTS:
After the treatment of non-transfected cells with gemcitabine, NF-
κ
B and AKT activities were increased, which may have induced the OSCC resistance to gemcitabine. Then, we found that TGF-
β
downregulation effectively reduced NF-
κ
B and AKT phosphorylation levels after the administration of gemcitabine and increased the OSCC sensitivity to gemcitabine, resulting in cell death and the blunting of OSCC resistance to gemcitabine. The EMT was also reduced by TGF-
β
downregulation combined with gemcitabine treatment.
CONCLUSION:
Cellular levels of TGF-
β
constitute an important factor in gemcitabine resistance and TGF-
β
silencing might represent a novel and potent strategy for overcoming OSCC resistance to gemcitabine.</abstract><cop>London, England</cop><pub>SAGE Publications</pub><doi>10.3233/CBM-201456</doi><tpages>9</tpages></addata></record> |
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| ispartof | Cancer biomarkers : section A of Disease markers, 2020-01, Vol.29 (2), p.179-187 |
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| source | Sage Journals GOLD Open Access 2024 |
| subjects | AKT protein Animal research Cancer Cell death Enzyme-linked immunosorbent assay Gemcitabine Growth factors Oral cancer Oral squamous cell carcinoma Phosphorylation Resistance factors Ribonucleic acid RNA Squamous cell carcinoma Transforming growth factor-b |
| title | TGF- β downregulation overcomes gemcitabine resistance in oral squamous cell carcinoma |
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