The Roles and Regulation of m6A Modification in Glioblastoma Stem Cells and Tumorigenesis

被引:7
作者
Li, Peng [1 ]
Richard, Hope T. [2 ]
Zhu, Kezhou [1 ]
Li, Linlin [1 ]
Huang, Suyun [1 ,3 ,4 ]
机构
[1] Virginia Commonwealth Univ, Sch Med, Dept Human & Mol Genet, Richmond, VA 23298 USA
[2] Virginia Commonwealth Univ, Sch Med, Dept Pathol, Richmond, VA 23298 USA
[3] Virginia Commonwealth Univ, Sch Med, Inst Mol Med, Richmond, VA 23298 USA
[4] Virginia Commonwealth Univ, VCU Massey Canc Ctr, Richmond, VA 23298 USA
关键词
m(6)A modification; glioblastoma; epigenetics; methyltransferase; demethylase; inhibitor; MESSENGER-RNA; NUCLEAR-RNA; SELF-RENEWAL; EXPRESSION; PROLIFERATION; TRANSLATION; BINDING; PROTEIN; MAINTENANCE; PROGRESSION;
D O I
10.3390/biomedicines10050969
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Glioblastoma is the most common and most lethal primary malignant brain tumor. N-6-methyladenosine (m(6)A) is a widespread and abundant internal messenger RNA (mRNA) modification found in eukaryotes. Accumulated evidence demonstrates that m(6)A modification is aberrantly activated in human cancers and is critical for tumorigenesis and metastasis. m(6)A modification is also strongly involved in key signaling pathways and is associated with prognosis in glioblastoma. Here, we briefly outline the functions of m(6)A and its regulatory proteins, including m(6)A writers, erasers, and readers of the fate of RNA. We also summarize the latest breakthroughs in this field, describe the underlying molecular mechanisms that contribute to the tumorigenesis and progression, and highlight the inhibitors targeting the factors in m(6)A modification in glioblastoma. Further studies focusing on the specific pathways of m(6)A modification could help identify biomarkers and therapeutic targets that might prevent and treat glioblastoma.
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页数:16
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