AXL is crucial for E1A‐enhanced therapeutic efficiency of EGFR tyrosine kinase inhibitors through NFI in breast cancer
AXL which is a chemosensitizer protein for breast cancer cells in response to epidermal growth factor receptor‐tyrosine kinase inhibitor and suppresses tumor growth. The clinical information show nuclear factor I (NFI)‐C and NFI‐X expression correlate with AXL expression in breast cancer patients. F...
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| Veröffentlicht in: | Environmental toxicology 2021-07, Vol.36 (7), p.1278-1287 |
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| creator | Su, Chih‐Ming Hsu, Tung‐Wei Sung, Shian‐Ying Huang, Ming‐Te Chen, Kuan‐Chou Huang, Chih‐Yang Chiang, Chien Yi Su, Yen‐Hao Chen, Hsin‐An Liao, Po‐Hsiang |
| description | AXL which is a chemosensitizer protein for breast cancer cells in response to epidermal growth factor receptor‐tyrosine kinase inhibitor and suppresses tumor growth. The clinical information show nuclear factor I (NFI)‐C and NFI‐X expression correlate with AXL expression in breast cancer patients. Following, we establish serial deletions of AXL promoter to identify regions required for Adenovirus‐5 early region 1A (E1A)‐mediated AXL suppression. All of the NFI family members were extensively studied for their expression and functions in regulating AXL. Moreover, E1A post‐transcriptionally downregulates AXL expression through NFI. NFI‐C and NFI‐X, not NFI‐A and NFI‐B, resulting in cell death in response to EGFR‐TKI. Our finding suggests that NFI‐C and NFI‐X are crucial regulators for AXL and significantly correlated with poor survival of breast cancer patients. |
| doi_str_mv | 10.1002/tox.23125 |
| format | Article |
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The clinical information show nuclear factor I (NFI)‐C and NFI‐X expression correlate with AXL expression in breast cancer patients. Following, we establish serial deletions of AXL promoter to identify regions required for Adenovirus‐5 early region 1A (E1A)‐mediated AXL suppression. All of the NFI family members were extensively studied for their expression and functions in regulating AXL. Moreover, E1A post‐transcriptionally downregulates AXL expression through NFI. NFI‐C and NFI‐X, not NFI‐A and NFI‐B, resulting in cell death in response to EGFR‐TKI. Our finding suggests that NFI‐C and NFI‐X are crucial regulators for AXL and significantly correlated with poor survival of breast cancer patients.</description><identifier>ISSN: 1520-4081</identifier><identifier>EISSN: 1522-7278</identifier><identifier>DOI: 10.1002/tox.23125</identifier><identifier>PMID: 33734566</identifier><language>eng</language><publisher>Hoboken, USA: John Wiley & Sons, Inc</publisher><subject>AXL ; Axl protein ; Breast cancer ; Breast Neoplasms - drug therapy ; Breast Neoplasms - genetics ; Cancer ; Cell death ; Cell Line, Tumor ; Drug Resistance, Neoplasm ; Early region ; EGFR tyrosine kinase inhibitor ; Enzyme inhibitors ; Epidermal growth factor ; Epidermal growth factor receptors ; ErbB Receptors - genetics ; Growth factors ; Humans ; Kinases ; Neoplasms ; NFI Transcription Factors ; Nuclear factor I ; Protein Kinase Inhibitors - pharmacology ; Protein Kinase Inhibitors - therapeutic use ; Proto-Oncogene Proteins - genetics ; Receptor Protein-Tyrosine Kinases - genetics ; Survival ; Transcription ; Tyrosine ; Tyrosine kinase inhibitors</subject><ispartof>Environmental toxicology, 2021-07, Vol.36 (7), p.1278-1287</ispartof><rights>2021 Wiley Periodicals LLC.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3905-3060187ea8f4371479238d60d69da4f13fc4e851296e0bf19fff695ae5470bee3</citedby><cites>FETCH-LOGICAL-c3905-3060187ea8f4371479238d60d69da4f13fc4e851296e0bf19fff695ae5470bee3</cites><orcidid>0000-0002-4266-5428 ; 0000-0003-2347-0411</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Ftox.23125$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Ftox.23125$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33734566$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Su, Chih‐Ming</creatorcontrib><creatorcontrib>Hsu, Tung‐Wei</creatorcontrib><creatorcontrib>Sung, Shian‐Ying</creatorcontrib><creatorcontrib>Huang, Ming‐Te</creatorcontrib><creatorcontrib>Chen, Kuan‐Chou</creatorcontrib><creatorcontrib>Huang, Chih‐Yang</creatorcontrib><creatorcontrib>Chiang, Chien Yi</creatorcontrib><creatorcontrib>Su, Yen‐Hao</creatorcontrib><creatorcontrib>Chen, Hsin‐An</creatorcontrib><creatorcontrib>Liao, Po‐Hsiang</creatorcontrib><title>AXL is crucial for E1A‐enhanced therapeutic efficiency of EGFR tyrosine kinase inhibitors through NFI in breast cancer</title><title>Environmental toxicology</title><addtitle>Environ Toxicol</addtitle><description>AXL which is a chemosensitizer protein for breast cancer cells in response to epidermal growth factor receptor‐tyrosine kinase inhibitor and suppresses tumor growth. The clinical information show nuclear factor I (NFI)‐C and NFI‐X expression correlate with AXL expression in breast cancer patients. Following, we establish serial deletions of AXL promoter to identify regions required for Adenovirus‐5 early region 1A (E1A)‐mediated AXL suppression. All of the NFI family members were extensively studied for their expression and functions in regulating AXL. Moreover, E1A post‐transcriptionally downregulates AXL expression through NFI. NFI‐C and NFI‐X, not NFI‐A and NFI‐B, resulting in cell death in response to EGFR‐TKI. Our finding suggests that NFI‐C and NFI‐X are crucial regulators for AXL and significantly correlated with poor survival of breast cancer patients.</description><subject>AXL</subject><subject>Axl protein</subject><subject>Breast cancer</subject><subject>Breast Neoplasms - drug therapy</subject><subject>Breast Neoplasms - genetics</subject><subject>Cancer</subject><subject>Cell death</subject><subject>Cell Line, Tumor</subject><subject>Drug Resistance, Neoplasm</subject><subject>Early region</subject><subject>EGFR tyrosine kinase inhibitor</subject><subject>Enzyme inhibitors</subject><subject>Epidermal growth factor</subject><subject>Epidermal growth factor receptors</subject><subject>ErbB Receptors - genetics</subject><subject>Growth factors</subject><subject>Humans</subject><subject>Kinases</subject><subject>Neoplasms</subject><subject>NFI Transcription Factors</subject><subject>Nuclear factor I</subject><subject>Protein Kinase Inhibitors - pharmacology</subject><subject>Protein Kinase Inhibitors - therapeutic use</subject><subject>Proto-Oncogene Proteins - genetics</subject><subject>Receptor Protein-Tyrosine Kinases - genetics</subject><subject>Survival</subject><subject>Transcription</subject><subject>Tyrosine</subject><subject>Tyrosine kinase inhibitors</subject><issn>1520-4081</issn><issn>1522-7278</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kcFO3DAQhq2qqMC2h75AZamXcgiM7dhJjiu0C0grkCoqcYscZ9w1zcZbO1HZG4_AM_IkmF3oAYmTR9Y3n2bmJ-Qrg2MGwE8Gf3fMBePyAzlgkvOs4EX5cVtDlkPJ9slhjLcAUCmpPpF9IQqRS6UOyN30ZkFdpCaMxumOWh_ojE0f7x-wX-reYEuHJQa9xnFwhqK1zjjszYZ6S2dn85902AQfXY_0j-t1ROr6pWvc4ENMncGPv5f0cn6RvmkTUMeBmmdt-Ez2rO4ifnl5J-TXfHZ9ep4trs4uTqeLzIgKZCZAASsL1KXNRcHyouKibBW0qmp1bpmwJsdSMl4phMayylqrKqlR5gU0iGJCfuy86-D_jhiHeuWiwa7TPfox1lwCL6EqVJ7Q72_QWz-GPk2XKKE4gCxZoo52lEl7x4C2Xge30mFTM6if46hTHPU2jsR-ezGOzQrb_-Tr_RNwsgP-uQ4375vq66ubnfIJtTiUEg</recordid><startdate>202107</startdate><enddate>202107</enddate><creator>Su, Chih‐Ming</creator><creator>Hsu, Tung‐Wei</creator><creator>Sung, Shian‐Ying</creator><creator>Huang, Ming‐Te</creator><creator>Chen, Kuan‐Chou</creator><creator>Huang, Chih‐Yang</creator><creator>Chiang, Chien Yi</creator><creator>Su, Yen‐Hao</creator><creator>Chen, Hsin‐An</creator><creator>Liao, Po‐Hsiang</creator><general>John Wiley & Sons, Inc</general><general>Wiley Subscription Services, Inc</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>7QH</scope><scope>7ST</scope><scope>7TN</scope><scope>7U7</scope><scope>7UA</scope><scope>C1K</scope><scope>F1W</scope><scope>H97</scope><scope>K9.</scope><scope>L.G</scope><scope>M7N</scope><scope>SOI</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-4266-5428</orcidid><orcidid>https://orcid.org/0000-0003-2347-0411</orcidid></search><sort><creationdate>202107</creationdate><title>AXL is crucial for E1A‐enhanced therapeutic efficiency of EGFR tyrosine kinase inhibitors through NFI in breast cancer</title><author>Su, Chih‐Ming ; 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The clinical information show nuclear factor I (NFI)‐C and NFI‐X expression correlate with AXL expression in breast cancer patients. Following, we establish serial deletions of AXL promoter to identify regions required for Adenovirus‐5 early region 1A (E1A)‐mediated AXL suppression. All of the NFI family members were extensively studied for their expression and functions in regulating AXL. Moreover, E1A post‐transcriptionally downregulates AXL expression through NFI. NFI‐C and NFI‐X, not NFI‐A and NFI‐B, resulting in cell death in response to EGFR‐TKI. Our finding suggests that NFI‐C and NFI‐X are crucial regulators for AXL and significantly correlated with poor survival of breast cancer patients.</abstract><cop>Hoboken, USA</cop><pub>John Wiley & Sons, Inc</pub><pmid>33734566</pmid><doi>10.1002/tox.23125</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0002-4266-5428</orcidid><orcidid>https://orcid.org/0000-0003-2347-0411</orcidid></addata></record> |
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| subjects | AXL Axl protein Breast cancer Breast Neoplasms - drug therapy Breast Neoplasms - genetics Cancer Cell death Cell Line, Tumor Drug Resistance, Neoplasm Early region EGFR tyrosine kinase inhibitor Enzyme inhibitors Epidermal growth factor Epidermal growth factor receptors ErbB Receptors - genetics Growth factors Humans Kinases Neoplasms NFI Transcription Factors Nuclear factor I Protein Kinase Inhibitors - pharmacology Protein Kinase Inhibitors - therapeutic use Proto-Oncogene Proteins - genetics Receptor Protein-Tyrosine Kinases - genetics Survival Transcription Tyrosine Tyrosine kinase inhibitors |
| title | AXL is crucial for E1A‐enhanced therapeutic efficiency of EGFR tyrosine kinase inhibitors through NFI in breast cancer |
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