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Olig2 regulates p53-mediated apoptosis, migration and invasion of melanoma cells

DC FieldValueLanguage
dc.contributor.author남기택-
dc.date.accessioned2021-04-29T17:37:17Z-
dc.date.available2021-04-29T17:37:17Z-
dc.date.issued2021-04-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/182437-
dc.description.abstractMelanoma is a disease with a high recurrence rate and poor prognosis; therefore, the need for targeted therapeutics is steadily increasing. Oligodendrocyte transcription factor2 (Olig2) is a basic helix-loop-helix transcription factor that is expressed in the central nervous system during embryonic development. Olig2 is overexpressed in various malignant cell lines such as lung carcinoma, glioma and melanoma. Olig2 is known as a key transcription factor that promotes tumor growth in malignant glioma. However, the role of Olig2 in melanoma is not well characterized. We analyzed the role of Olig2 in apoptosis, migration, and invasion of melanoma cells. We confirmed that Olig2 was overexpressed in melanoma cells and tissues. Reduction of Olig2 increased apoptosis in melanoma cells by increasing p53 level and caspase-3/-7 enzyme activity. In addition, downregulation of Olig2 suppressed migration and invasion of melanoma cells by inhibiting EMT. Reduction of Olig2 inhibited expression of MMP-1 and the enzyme activity of MMP-2/-9 induced by TGF-β. Moreover, Olig2 was involved in the downstream stages of MEK/ERK and PI3K/AKT, which are major signaling pathways in metastatic progression of melanoma. In conclusion, this study demonstrated the crucial roles of Olig2 in apoptosis, migration, and invasion of melanoma and may help to further our understanding of the relationship between Olig2 and melanoma progression.-
dc.description.statementOfResponsibilityopen-
dc.languageEnglish-
dc.publisherNature Publishing Group-
dc.relation.isPartOfSCIENTIFIC REPORTS-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.titleOlig2 regulates p53-mediated apoptosis, migration and invasion of melanoma cells-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentBioMedical Science Institute (의생명과학부)-
dc.contributor.googleauthorJi Eun Lee-
dc.contributor.googleauthorSungjin Ahn-
dc.contributor.googleauthorHaengdueng Jeong-
dc.contributor.googleauthorSeungchan An-
dc.contributor.googleauthorCheol Hwan Myung-
dc.contributor.googleauthorJeong Ah Lee-
dc.contributor.googleauthorSung Chan Hong-
dc.contributor.googleauthorYoun Jin Kim-
dc.contributor.googleauthorJin Young Kim-
dc.contributor.googleauthorJong Hyuk Ryu-
dc.contributor.googleauthorMinsoo Noh-
dc.contributor.googleauthorKi Taek Nam-
dc.contributor.googleauthorJae Sung Hwang-
dc.identifier.doi10.1038/s41598-021-87438-x-
dc.contributor.localIdA01243-
dc.relation.journalcodeJ02646-
dc.identifier.eissn2045-2322-
dc.identifier.pmid33833342-
dc.contributor.alternativeNameNam, Ki Taek-
dc.contributor.affiliatedAuthor남기택-
dc.citation.volume11-
dc.citation.number1-
dc.citation.startPage7778-
dc.identifier.bibliographicCitationSCIENTIFIC REPORTS, Vol.11(1) : 7778, 2021-04-
Appears in Collections:
1. College of Medicine (의과대학) > BioMedical Science Institute (의생명과학부) > 1. Journal Papers

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