期刊
ONCOTARGET
卷 7, 期 31, 页码 49450-49458出版社
IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.10370
关键词
EZH2; miRNA; beta-catenin; aerobic glycolysis; glioma
资金
- Research Special Fund For Public Welfare Industry of Health [201402008]
- National High Technology Research and Development Program of China (863) [2012AA02A508]
- National Natural Science Foundation of China [81472362, 81372709, 81302185]
- Jiangsu Province's Natural Science Foundation [BK20131019, BK20151585]
- Program for Advanced Talents within Six Industries of Jiangsu Province [2015-WSN-036]
- Jiangsu Province's Key Provincial Talents Program [RC2011051]
- Jiangsu Province's Key Discipline of Medicine [XK201117]
- Program for Development of Innovative Research Team in the First Affiliated Hospital of NJMU
- Priority Academic Program Development of Jiangsu Higher Education Institutions (PAPD)
EZH2 is up-regulated in various cancer types, implicating its role in tumorigenesis. Our recent data have shown that repression of EZH2 inhibited glioma growth by inhibition beta-catenin signaling. Here, we identified several miRNAs that were repressed by EZH2, which in turn regulate beta-catenin expression by its 3'UTR, such as miR-1224-3p, miR-328 and miR-214. Further, EZH2 silenced miR-328 expression by binding to miR-328 promoter and promoting methylation of miR-328 promoter. Finally, miR-328 largely abrogated EZH2 effects on beta-catenin expression and glucose metabolism in glioma cells. Taken together, we propose a model for a coordinated EZH2-beta-catenin oncoprotein axis, and epigenetic link between histone modification and DNA methylation, mediated by EZH2-scilenced miRNAs.
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