Cited 12 times in
Inhibition of Chk1 by miR-320c increases oxaliplatin responsiveness in triple-negative breast cancer
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 강혁구 | - |
dc.contributor.author | 전경희 | - |
dc.date.accessioned | 2020-12-01T17:43:13Z | - |
dc.date.available | 2020-12-01T17:43:13Z | - |
dc.date.issued | 2020-10 | - |
dc.identifier.uri | https://ir.ymlib.yonsei.ac.kr/handle/22282913/180403 | - |
dc.description.abstract | Checkpoint kinase 1 (Chk1) expression is enhanced in most cancers owing to oncogenic activation and constant replicative stress. Chk1 inactivation is a promising cancer therapy, as its inactivation leads to genomic instability, chromosomal catastrophe, and cancer cell death. Herein, we observed that miR-320c, downregulated in triple-negative breast cancer (TNBC) patients, can target Chk1. In addition, downregulated miR-320c expression was associated with poor overall survival in TNBC patients. As Chk1 was associated with the DNA damage response (DDR), we investigated the effect of miR-320c on DDR in TNBC cells. To induce DNA damage, we used platinum-based drugs, especially oxaliplatin, which is most effective with miR-320c. We observed that overexpression of miR-320c in TNBC regulated the oxaliplatin responsiveness by mediating DNA damage repair through the negative regulation of Chk1 in vitro. Furthermore, using a xenograft model, a combination of miR-320c mimic and oxaliplatin effectively inhibited tumor progression. These investigations indicate the potential of miR-320c as a marker of oxaliplatin responsiveness and a therapeutic target to increase the efficacy of chemotherapy in TNBC. | - |
dc.description.statementOfResponsibility | open | - |
dc.format | application/pdf | - |
dc.language | English | - |
dc.publisher | Nature Pub. Group | - |
dc.relation.isPartOf | ONCOGENESIS | - |
dc.rights | CC BY-NC-ND 2.0 KR | - |
dc.title | Inhibition of Chk1 by miR-320c increases oxaliplatin responsiveness in triple-negative breast cancer | - |
dc.type | Article | - |
dc.contributor.college | College of Medicine (의과대학) | - |
dc.contributor.department | Dept. of Biochemistry and Molecular Biology (생화학-분자생물학교실) | - |
dc.contributor.googleauthor | Sera Lim | - |
dc.contributor.googleauthor | Yesol Kim | - |
dc.contributor.googleauthor | Soo-Been Lee | - |
dc.contributor.googleauthor | Hyeok-Gu Kang | - |
dc.contributor.googleauthor | Da-Hyun Kim | - |
dc.contributor.googleauthor | Jee Won Park | - |
dc.contributor.googleauthor | Daeun Chung | - |
dc.contributor.googleauthor | Hyunkyung Kong | - |
dc.contributor.googleauthor | Kyung Hyun Yoo | - |
dc.contributor.googleauthor | Yonghwan Kim | - |
dc.contributor.googleauthor | Wonshik Han | - |
dc.contributor.googleauthor | Kyung-Hee Chun | - |
dc.contributor.googleauthor | Jong Hoon Park | - |
dc.identifier.doi | 10.1038/s41389-020-00275-x | - |
dc.contributor.localId | A00090 | - |
dc.contributor.localId | A03501 | - |
dc.relation.journalcode | J02414 | - |
dc.identifier.eissn | 2157-9024 | - |
dc.identifier.pmid | 33041328 | - |
dc.contributor.alternativeName | Kang, Hyeok Gu | - |
dc.contributor.affiliatedAuthor | 강혁구 | - |
dc.contributor.affiliatedAuthor | 전경희 | - |
dc.citation.volume | 9 | - |
dc.citation.number | 10 | - |
dc.citation.startPage | 91 | - |
dc.identifier.bibliographicCitation | ONCOGENESIS, Vol.9(10) : 91, 2020-10 | - |
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.