MIR-27a regulates the TGF- signaling pathway by targeting SMAD2 and SMAD4 in lung cancer
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Chae, Dong-Kyu | - |
dc.contributor.author | Ban, Eunmi | - |
dc.contributor.author | Yoo, Young Sook | - |
dc.contributor.author | Kim, Eunice EunKyeong | - |
dc.contributor.author | Baik, Ja-Hyun | - |
dc.contributor.author | Song, Eun Joo | - |
dc.date.accessioned | 2021-09-03T03:21:11Z | - |
dc.date.available | 2021-09-03T03:21:11Z | - |
dc.date.created | 2021-06-16 | - |
dc.date.issued | 2017-08 | - |
dc.identifier.issn | 0899-1987 | - |
dc.identifier.uri | https://scholar.korea.ac.kr/handle/2021.sw.korea/82650 | - |
dc.description.abstract | The transforming growth factor- (TGF-) signaling pathway is associated with carcinogenesis and various biological processes. SMAD2 and SMAD4, which are putative tumor suppressors, have an important role in TGF- signaling. The aberrant expression of these genes is implicated in some cancers. However, the mechanisms of SMAD2 and SMAD4 dysregulation are poorly understood. In this study, we observed that miR-27a was upregulated in lung cancer cell lines and patients. In addition, SMAD2 and SMAD4 genes were identified as targets of miR-27a by several target prediction databases and experimental validation. Functional studies revealed that miR-27a overexpression decreased SMAD2 and SMAD4 mRNA and protein levels. Furthermore, miR-27a contributed to cell proliferation and invasion by inhibiting TGF--induced cell cycle arrest. These results suggest that miR-27a may function as an oncogene by regulating SMAD2 and SMAD4 in lung cancer. Thus, miR-27a may be a potential target for cancer therapy. | - |
dc.language | English | - |
dc.language.iso | en | - |
dc.publisher | WILEY | - |
dc.subject | MICRORNA-27A FUNCTIONS | - |
dc.subject | TUMOR-SUPPRESSOR | - |
dc.subject | PROGRESSION | - |
dc.subject | CARCINOMA | - |
dc.subject | CELLS | - |
dc.title | MIR-27a regulates the TGF- signaling pathway by targeting SMAD2 and SMAD4 in lung cancer | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Baik, Ja-Hyun | - |
dc.identifier.doi | 10.1002/mc.22655 | - |
dc.identifier.scopusid | 2-s2.0-85017505665 | - |
dc.identifier.wosid | 000404896500014 | - |
dc.identifier.bibliographicCitation | MOLECULAR CARCINOGENESIS, v.56, no.8, pp.1992 - 1998 | - |
dc.relation.isPartOf | MOLECULAR CARCINOGENESIS | - |
dc.citation.title | MOLECULAR CARCINOGENESIS | - |
dc.citation.volume | 56 | - |
dc.citation.number | 8 | - |
dc.citation.startPage | 1992 | - |
dc.citation.endPage | 1998 | - |
dc.type.rims | ART | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Biochemistry & Molecular Biology | - |
dc.relation.journalResearchArea | Oncology | - |
dc.relation.journalWebOfScienceCategory | Biochemistry & Molecular Biology | - |
dc.relation.journalWebOfScienceCategory | Oncology | - |
dc.subject.keywordPlus | MICRORNA-27A FUNCTIONS | - |
dc.subject.keywordPlus | TUMOR-SUPPRESSOR | - |
dc.subject.keywordPlus | PROGRESSION | - |
dc.subject.keywordPlus | CARCINOMA | - |
dc.subject.keywordPlus | CELLS | - |
dc.subject.keywordAuthor | lung cancer | - |
dc.subject.keywordAuthor | miR-27a | - |
dc.subject.keywordAuthor | SMAD2 | - |
dc.subject.keywordAuthor | SMAD4 | - |
dc.subject.keywordAuthor | TGF- | - |
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.
(02841) 서울특별시 성북구 안암로 14502-3290-1114
COPYRIGHT © 2021 Korea University. All Rights Reserved.
Certain data included herein are derived from the © Web of Science of Clarivate Analytics. All rights reserved.
You may not copy or re-distribute this material in whole or in part without the prior written consent of Clarivate Analytics.