2 474

Cited 12 times in

Inhibition of Chk1 by miR-320c increases oxaliplatin responsiveness in triple-negative breast cancer

DC Field Value Language
dc.contributor.author강혁구-
dc.contributor.author전경희-
dc.date.accessioned2020-12-01T17:43:13Z-
dc.date.available2020-12-01T17:43:13Z-
dc.date.issued2020-10-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/180403-
dc.description.abstractCheckpoint 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.statementOfResponsibilityopen-
dc.formatapplication/pdf-
dc.languageEnglish-
dc.publisherNature Pub. Group-
dc.relation.isPartOfONCOGENESIS-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.titleInhibition of Chk1 by miR-320c increases oxaliplatin responsiveness in triple-negative breast cancer-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Biochemistry and Molecular Biology (생화학-분자생물학교실)-
dc.contributor.googleauthorSera Lim-
dc.contributor.googleauthorYesol Kim-
dc.contributor.googleauthorSoo-Been Lee-
dc.contributor.googleauthorHyeok-Gu Kang-
dc.contributor.googleauthorDa-Hyun Kim-
dc.contributor.googleauthorJee Won Park-
dc.contributor.googleauthorDaeun Chung-
dc.contributor.googleauthorHyunkyung Kong-
dc.contributor.googleauthorKyung Hyun Yoo-
dc.contributor.googleauthorYonghwan Kim-
dc.contributor.googleauthorWonshik Han-
dc.contributor.googleauthorKyung-Hee Chun-
dc.contributor.googleauthorJong Hoon Park-
dc.identifier.doi10.1038/s41389-020-00275-x-
dc.contributor.localIdA00090-
dc.contributor.localIdA03501-
dc.relation.journalcodeJ02414-
dc.identifier.eissn2157-9024-
dc.identifier.pmid33041328-
dc.contributor.alternativeNameKang, Hyeok Gu-
dc.contributor.affiliatedAuthor강혁구-
dc.contributor.affiliatedAuthor전경희-
dc.citation.volume9-
dc.citation.number10-
dc.citation.startPage91-
dc.identifier.bibliographicCitationONCOGENESIS, Vol.9(10) : 91, 2020-10-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Biochemistry and Molecular Biology (생화학-분자생물학교실) > 1. Journal Papers

qrcode

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.