A Small Organic Molecule Blocks EGFR Transport into the Nucleus by the Nonclassical Pathway Resulting in Repression of Cancer Invasion
DC Field | Value | Language |
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dc.contributor.author | Ha, Siyoung | - |
dc.contributor.author | Jeong, Jangho | - |
dc.contributor.author | Oh, Jiwon | - |
dc.contributor.author | Rhee, Sangmyung | - |
dc.contributor.author | Ham, Seung Wook | - |
dc.date.available | 2019-01-22T14:13:45Z | - |
dc.date.issued | 2018-01 | - |
dc.identifier.issn | 1439-4227 | - |
dc.identifier.issn | 1439-7633 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/1313 | - |
dc.description.abstract | In addition to the traditional epidermal growth factor receptor (EGFR) signaling pathways, nuclear EGFR has been shown to control multiple cellular functions, including cell proliferation and invasion. It has been reported that EGFR is transported into the nucleus after forming a complex with KPNA/KPNB1 or KPNB1. Herein, it is shown that EGFR can interact with both KP and KPNA, but EGF-activated EGFR mostly binds with KPNB1 through the pull-down assay. Also, a small organic molecule (1), an effective binder of KPNB1, inhibits the interaction between EGFR and KPNB1 in the nonclassical transport pathway, but not KPNA. Furthermore, treatment of cancer cells with 1 noticeably blocks the nuclear entry of EGFR, which results in significant suppression of invasion by lung cancer H1299 cells. These findings show that 1 is an effective inhibitor of EGFR/KPNB1 interactions in vitro, it may be used in cellular studies as a tool to determine the role of nuclear EGFR, and it is a drug candidate. | - |
dc.format.extent | 5 | - |
dc.language | 영어 | - |
dc.language.iso | ENG | - |
dc.publisher | WILEY-V C H VERLAG GMBH | - |
dc.title | A Small Organic Molecule Blocks EGFR Transport into the Nucleus by the Nonclassical Pathway Resulting in Repression of Cancer Invasion | - |
dc.type | Article | - |
dc.identifier.doi | 10.1002/cbic.201700489 | - |
dc.identifier.bibliographicCitation | CHEMBIOCHEM, v.19, no.2, pp 131 - 135 | - |
dc.description.isOpenAccess | N | - |
dc.identifier.wosid | 000422716300005 | - |
dc.identifier.scopusid | 2-s2.0-85037997846 | - |
dc.citation.endPage | 135 | - |
dc.citation.number | 2 | - |
dc.citation.startPage | 131 | - |
dc.citation.title | CHEMBIOCHEM | - |
dc.citation.volume | 19 | - |
dc.type.docType | Article | - |
dc.publisher.location | 영국 | - |
dc.subject.keywordAuthor | aminothiazoles | - |
dc.subject.keywordAuthor | cancer | - |
dc.subject.keywordAuthor | inhibitor | - |
dc.subject.keywordAuthor | nuclear transport | - |
dc.subject.keywordAuthor | receptors | - |
dc.subject.keywordPlus | GROWTH-FACTOR RECEPTOR | - |
dc.subject.keywordPlus | IMPORTIN-BETA | - |
dc.subject.keywordPlus | LUNG-CANCER | - |
dc.subject.keywordPlus | RADIATION SENSITIVITY | - |
dc.subject.keywordPlus | LOCALIZATION SEQUENCE | - |
dc.subject.keywordPlus | PROTEIN EXPRESSION | - |
dc.subject.keywordPlus | NITRIC-OXIDE | - |
dc.subject.keywordPlus | DNA-PK | - |
dc.subject.keywordPlus | TRANSLOCATION | - |
dc.subject.keywordPlus | CELLS | - |
dc.relation.journalResearchArea | Biochemistry & Molecular Biology | - |
dc.relation.journalResearchArea | Pharmacology & Pharmacy | - |
dc.relation.journalWebOfScienceCategory | Biochemistry & Molecular Biology | - |
dc.relation.journalWebOfScienceCategory | Chemistry, Medicinal | - |
dc.description.journalRegisteredClass | sci | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
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