期刊
CANCER CELL
卷 31, 期 4, 页码 591-+出版社
CELL PRESS
DOI: 10.1016/j.ccell.2017.02.013
关键词
-
资金
- US NIH [R01CA157933, R01CA182684, R01CA201327, R01CA152309, CA16672, GM071440]
The dynamic and reversible N-6-methyladenosine (m(6)A) RNA modification installed and erased by N-6-methyltransferases and demethylases regulates gene expression and cell fate. We show that the m(6)A demethylase ALKBH5 is highly expressed in glioblastoma stem-like cells (GSCs). Silencing ALKBH5 suppresses the proliferation of patient-derived GSCs. Integrated transcriptome and m(6)A-seq analyses revealed altered expression of certain ALKBH5 target genes, including the transcription factor FOXM1. ALKBH5 demethylates FOXM1 nascent transcripts, leading to enhanced FOXM1 expression. Furthermore, a long non-coding RNA antisense to FOXM1 (FOXM1-AS) promotes the interaction of ALKBH5 with FOXM1 nascent transcripts. Depleting ALKBH5 and FOXM1-AS disrupted GSC tumorigenesis through the FOXM1 axis. Our work uncovers a critical function for ALKBH5 and provides insight into critical roles of m(6)A methylation in glioblastoma.
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