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Competing Endogenous RNA of Snail and Zeb1 UTR in Therapeutic Resistance of Colorectal Cancer

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dc.contributor.author김남희-
dc.contributor.author김현실-
dc.contributor.author육종인-
dc.contributor.author차소영-
dc.contributor.author김현실-
dc.contributor.author육종인-
dc.contributor.author차소영-
dc.date.accessioned2021-09-29T02:19:02Z-
dc.date.available2021-09-29T02:19:02Z-
dc.date.issued2021-09-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/184825-
dc.description.abstractThe epithelial-mesenchymal transition (EMT) comprises an important biological mechanism not only for cancer progression but also in the therapeutic resistance of cancer cells. While the importance of the protein abundance of EMT-inducers, such as Snail (SNAI1) and Zeb1 (ZEB1), during EMT progression is clear, the reciprocal interactions between the untranslated regions (UTRs) of EMT-inducers via a competing endogenous RNA (ceRNA) network have received little attention. In this study, we found a synchronized transcript abundance of Snail and Zeb1 mediated by a non-coding RNA network in colorectal cancer (CRC). Importantly, the trans-regulatory ceRNA network in the UTRs of EMT inducers is mediated by competition between tumor suppressive miRNA-34 (miR-34) and miRNA-200 (miR-200). Furthermore, the ceRNA network consisting of the UTRs of EMT inducers and tumor suppressive miRs is functional in the EMT phenotype and therapeutic resistance of colon cancer. In The Cancer Genome Atlas (TCGA) samples, we also found genome-wide ceRNA gene sets regulated by miR-34a and miR-200 in colorectal cancer. These results indicate that the ceRNA networks regulated by the reciprocal interaction between EMT gene UTRs and tumor suppressive miRs are functional in CRC progression and therapeutic resistance.-
dc.description.statementOfResponsibilityopen-
dc.languageEnglish-
dc.publisherMDPI-
dc.relation.isPartOfINTERNATIONAL JOURNAL OF MOLECULAR SCIENCES-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.titleCompeting Endogenous RNA of Snail and Zeb1 UTR in Therapeutic Resistance of Colorectal Cancer-
dc.typeArticle-
dc.contributor.collegeCollege of Dentistry (치과대학)-
dc.contributor.departmentResearch Institute (부설연구소)-
dc.contributor.googleauthorNam Hee Kim-
dc.contributor.googleauthorSang Hyun Song-
dc.contributor.googleauthorYun Hee Choi-
dc.contributor.googleauthorKyu Ho Hwang-
dc.contributor.googleauthorJun Seop Yun-
dc.contributor.googleauthorHyeeun Song-
dc.contributor.googleauthorSo Young Cha-
dc.contributor.googleauthorSue Bean Cho-
dc.contributor.googleauthorInhan Lee-
dc.contributor.googleauthorHyun Sil Kim-
dc.contributor.googleauthorJong In Yook-
dc.identifier.doi10.3390/ijms22179589-
dc.contributor.localIdA00360-
dc.contributor.localIdA01121-
dc.contributor.localIdA02536-
dc.contributor.localIdA03997-
dc.contributor.localIdA01121-
dc.contributor.localIdA02536-
dc.contributor.localIdA03997-
dc.relation.journalcodeJ01133-
dc.identifier.eissn1422-0067-
dc.identifier.pmid34502497-
dc.subject.keywordSnail-
dc.subject.keywordZEB1-
dc.subject.keywordceRNA-
dc.subject.keywordcolorectal cancer-
dc.subject.keywordepithelial mesenchymal transition-
dc.subject.keywordtherapeutic resistance-
dc.contributor.alternativeNameKim, Nam Hee-
dc.contributor.affiliatedAuthor김남희-
dc.contributor.affiliatedAuthor김현실-
dc.contributor.affiliatedAuthor육종인-
dc.contributor.affiliatedAuthor차소영-
dc.contributor.affiliatedAuthor김현실-
dc.contributor.affiliatedAuthor육종인-
dc.contributor.affiliatedAuthor차소영-
dc.citation.volume22-
dc.citation.number17-
dc.citation.startPage9589-
dc.identifier.bibliographicCitationINTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, Vol.22(17) : 9589, 2021-09-
Appears in Collections:
2. College of Dentistry (치과대학) > Research Institute (부설연구소) > 1. Journal Papers
2. College of Dentistry (치과대학) > Dept. of Oral Pathology (구강병리학교실) > 1. Journal Papers

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