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METTL3 regulates alternative splicing of cell cycle-related genes via crosstalk between mRNA m(6)A modifications and splicing factors

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dc.contributor.authorKim, Yeongjoo-
dc.contributor.authorShin, Seungjae-
dc.contributor.authorKwon, Sunyoung-
dc.contributor.authorMoon, Kisung-
dc.contributor.authorBaek, Su -Vin-
dc.contributor.authorJo, Ahyoung-
dc.contributor.authorKim, Hyung-Sik-
dc.contributor.authorHwang, Gue-Ho-
dc.contributor.authorBae, Sang Su-
dc.contributor.authorKim, Yun Hak-
dc.contributor.authorCho, Sung Yup-
dc.contributor.authorOh, Jung-Min-
dc.date.accessioned2024-05-16T01:37:27Z-
dc.date.available2024-05-16T01:37:27Z-
dc.date.created2023-06-19-
dc.date.created2023-06-19-
dc.date.created2023-06-19-
dc.date.issued2023-04-
dc.identifier.citationAmerican Journal of Cancer Research, Vol.13 No.4, pp.1443-1456-
dc.identifier.issn2156-6976-
dc.identifier.urihttps://hdl.handle.net/10371/202727-
dc.description.abstractN-6-methyladenosine (m(6)A) modification in RNA affects various aspects of RNA metabolism and regulates gene expression. This modification is modulated by many regulatory proteins, such as m(6)A methyltransferases (writ-ers), m(6)A demethylases (erasers), and m(6)A-binding proteins (readers). Previous studies have suggested that al-terations in m6A regulatory proteins induce genome-wide alternative splicing in many cancer cells. However, the functional effects and molecular mechanisms of m6A-mediated alternative splicing have not been fully elucidated. To understand the consequences of this modification on RNA splicing in cancer cells, we performed RNA sequenc-ing and analyzed alternative splicing patterns in METTL3-knockdown osteosarcoma U2OS cells. We detected 1,803 alternatively spliced genes in METTL3-knockdown cells compared to the controls and found that cell cycle-related genes were enriched in differentially spliced genes. A comparison of the published MeRIP-seq data for METTL14 with our RNA sequencing data revealed that 70-87% of alternatively spliced genes had an m6A peak near 1 kb of alternative splicing sites. Among the 19 RNA-binding proteins enriched in alternative splicing sites, as revealed by motif analysis, expression of SFPQ highly correlated with METTL3 expression in 12,839 TCGA pan-cancer patients. We also found that cell cycle-related genes were enriched in alternatively spliced genes of other cell lines with METTL3 knockdown. Taken together, we suggest that METTL3 regulates m(6)A-dependent alternative splicing, espe-cially in cell cycle-related genes, by regulating the functions of splicing factors such as SFPQ.-
dc.language영어-
dc.publishere-Century Publishing Corporation-
dc.titleMETTL3 regulates alternative splicing of cell cycle-related genes via crosstalk between mRNA m(6)A modifications and splicing factors-
dc.typeArticle-
dc.citation.journaltitleAmerican Journal of Cancer Research-
dc.identifier.wosid000982232900018-
dc.citation.endpage1456-
dc.citation.number4-
dc.citation.startpage1443-
dc.citation.volume13-
dc.description.isOpenAccessN-
dc.contributor.affiliatedAuthorBae, Sang Su-
dc.contributor.affiliatedAuthorCho, Sung Yup-
dc.type.docTypeArticle-
dc.description.journalClass1-
dc.subject.keywordPlusPLOTTING SERVER-
dc.subject.keywordPlusMAP ANALYSIS-
dc.subject.keywordPlusNUCLEAR-RNA-
dc.subject.keywordPlusN-6-METHYLADENOSINE-
dc.subject.keywordPlusRECOGNITION-
dc.subject.keywordPlusTRANSLATION-
dc.subject.keywordPlusMUTATIONS-
dc.subject.keywordPlusCOMPLEX-
dc.subject.keywordPlusPSF-
dc.subject.keywordAuthorAlternative splicing-
dc.subject.keywordAuthorcell cycle-
dc.subject.keywordAuthorm6A modification-
dc.subject.keywordAuthorMETTL3-
dc.subject.keywordAuthorsplicing factor-
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Research Area Cancer genomics, Drug resistance, Targeted therapeutics

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