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Large-scale pharmacogenomics based drug discovery for ITGB3 dependent chemoresistance in mesenchymal lung cancer
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Hong, Soon-Ki | - |
dc.contributor.author | Lee, Haeseung | - |
dc.contributor.author | Kwon, Ok-Seon | - |
dc.contributor.author | Song, Na-Young | - |
dc.contributor.author | Lee, Hyo-Ju | - |
dc.contributor.author | Kang, Seungmin | - |
dc.contributor.author | Kim, Jeong-Hwan | - |
dc.contributor.author | Kim, Mirang | - |
dc.contributor.author | Kim, Wankyu | - |
dc.contributor.author | Cha, Hyuk-Jin | - |
dc.date.accessioned | 2019-03-13T01:45:32Z | - |
dc.date.available | 2019-03-13T10:46:54Z | - |
dc.date.issued | 2018-12-18 | - |
dc.identifier.citation | Molecular Cancer, 17(1):175 | ko_KR |
dc.identifier.issn | 1476-4598 | - |
dc.identifier.uri | https://hdl.handle.net/10371/147069 | - |
dc.description.abstract | Even when targets responsible for chemoresistance are identified, drug development is often hampered due to the poor druggability of these proteins. We systematically analyzed therapy-resistance with a large-scale cancer cell transcriptome and drug-response datasets and predicted the candidate drugs based on the gene expression profile. Our results implicated the epithelial–mesenchymal transition as a common mechanism underlying resistance to chemotherapeutic drugs. Notably, we identified ITGB3, whose expression was abundant in both drug resistance and mesenchymal status, as a promising target to overcome chemoresistance. We also confirmed that depletion of ITGB3 sensitized cancer cells to conventional chemotherapeutic drugs by modulating the NF-κB signaling pathway. Considering the poor druggability of ITGB3 and the lack of feasible drugs to directly inhibit this protein, we took an in silico screening for drugs mimicking the transcriptome-level changes caused by knockdown of ITGB3. This approach successfully identified atorvastatin as a novel candidate for drug repurposing, paving an alternative path to drug screening that is applicable to undruggable targets. | ko_KR |
dc.description.sponsorship | This work was supported by a grant from the National Research Foundation of Korea (NRF-2017M3C9A5028691 from HJC, NRF-2017M3C9A5028690 from WKK and NRF-2017R1A6A3A11030794 from HSL). | ko_KR |
dc.language.iso | en | ko_KR |
dc.publisher | BioMed Central | ko_KR |
dc.subject | Chemoresistance | ko_KR |
dc.subject | Mesenchymal cancer | ko_KR |
dc.subject | Pharmacogenomics | ko_KR |
dc.subject | Drug repurposing | ko_KR |
dc.subject | Biomarker | ko_KR |
dc.subject | ITGB3 | ko_KR |
dc.subject | NF-κB | ko_KR |
dc.subject | Atorvastatin | ko_KR |
dc.subject | Systems pharmacology | ko_KR |
dc.title | Large-scale pharmacogenomics based drug discovery for ITGB3 dependent chemoresistance in mesenchymal lung cancer | ko_KR |
dc.type | Article | ko_KR |
dc.contributor.AlternativeAuthor | 홍순기 | - |
dc.contributor.AlternativeAuthor | 이해승 | - |
dc.contributor.AlternativeAuthor | 권옥순 | - |
dc.contributor.AlternativeAuthor | 송나영 | - |
dc.contributor.AlternativeAuthor | 이효주 | - |
dc.contributor.AlternativeAuthor | 강승민 | - |
dc.contributor.AlternativeAuthor | 김정환 | - |
dc.contributor.AlternativeAuthor | 김미랑 | - |
dc.contributor.AlternativeAuthor | 김완규 | - |
dc.contributor.AlternativeAuthor | 차혁진 | - |
dc.identifier.doi | 10.1186/s12943-018-0924-8 | - |
dc.language.rfc3066 | en | - |
dc.rights.holder | The Author(s). | - |
dc.date.updated | 2018-12-23T04:15:42Z | - |
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