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STAT3-mediated MLST8 gene expression regulates cap-dependent translation in cancer cells

DC FieldValueLanguage
dc.contributor.author정호성-
dc.contributor.author김혜영-
dc.date.accessioned2020-09-30T16:45:59Z-
dc.date.available2020-09-30T16:45:59Z-
dc.date.issued2020-08-
dc.identifier.issn1574-7891-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/179614-
dc.description.abstractSignal transducer and activator of transcription 3 (STAT3) regulates cell growth, cell survival, angiogenesis, metastasis of cancer cells, and cancer immune evasion by regulating gene expression as a transcription factor. However, the effect of STAT3 on translation is almost unknown. We demonstrated that STAT3 acts as a trans-acting factor for MLST8 gene expression and the protein level of mLST8, a core component of mechanistic target of rapamycin complex 1 and 2 (mTORC1/2), positively regulates the mTORC1/2 downstream pathways. Suppression of STAT3 by siRNA attenuated 4E-BP1 phosphorylation, cap-dependent translation, and cell proliferation in a variety of cancer cells. In HCT116 cells, STAT3 knockdown-induced decreases in 4E-BP1 and AKT phosphorylation levels were further attenuated by MLST8 knockdown or recovered by mLST8 overexpression. STAT3 knockdown-induced G2/M phase arrest was partially restored by co-knockdown of 4EBP1, and the attenuation of cell proliferation was enhanced by the expression of an mTORC1-mediated phosphorylation-defective mutant of 4E-BP1. ChIP and promoter mapping using a luciferase reporter assay showed that the -951 to -894 bp of MLST8 promoter seems to include STAT3-binding site. Overall, these results suggest that STAT3-driven MLST8 gene expression regulates cap-dependent translation through 4E-BP1 phosphorylation in cancer cells.-
dc.description.statementOfResponsibilityopen-
dc.formatapplication/pdf-
dc.languageEnglish-
dc.publisherJohn Wiley & Sons, Inc-
dc.relation.isPartOfMOLECULAR ONCOLOGY-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.titleSTAT3-mediated MLST8 gene expression regulates cap-dependent translation in cancer cells-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Anatomy (해부학교실)-
dc.contributor.googleauthorHyunji Lee-
dc.contributor.googleauthorHyunjung Chin-
dc.contributor.googleauthorHyeyoung Kim-
dc.contributor.googleauthorHosung Jung-
dc.contributor.googleauthorDaekee Lee-
dc.identifier.doi10.1002/1878-0261.12735-
dc.contributor.localIdA03786-
dc.relation.journalcodeJ03480-
dc.identifier.eissn1878-0261-
dc.identifier.pmid32495998-
dc.subject.keyword4E-BP1-
dc.subject.keywordMLST8-
dc.subject.keywordSTAT3-
dc.subject.keywordcross-talk-
dc.subject.keywordmTORC1-
dc.contributor.alternativeNameJung, Ho Sung-
dc.contributor.affiliatedAuthor정호성-
dc.citation.volume14-
dc.citation.number8-
dc.citation.startPage1850-
dc.citation.endPage1867-
dc.identifier.bibliographicCitationMOLECULAR ONCOLOGY, Vol.14(8) : 1850-1867, 2020-08-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Anatomy (해부학교실) > 1. Journal Papers

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