期刊
CELL CYCLE
卷 13, 期 2, 页码 191-198出版社
TAYLOR & FRANCIS INC
DOI: 10.4161/cc.27646
关键词
miRNA; c-MYC; aggressive B-cell lymphomas; epigenetic; methylation
类别
资金
- National Cancer Institutes [R01 CA137123]
- Maher Fund
- Lymphoma Research Foundation
- National Functional Genomics Center Programmatic Research grand
- American Hematology Society
MYC (c-Myc) deregulation has been frequently associated with aggressive lymphomas and adverse clinical outcome in B-cell malignancies. MYC has been implicated in controlling the expression of miRNAs, and MYC-regulated miRNAs affect virtually all aspects of the hallmarks of MYC-driven lymphomas. Increasing evidence has indicated that there is significant cross-talk between MYC and miRNAs, with MYC regulating expression of a number of miRNAs, resulting in widespread repression of miRNA and, at the same time, MYC being subjected to regulation by miRNAs, leading to sustained MYC activity and the corresponding MYC downstream pathways. Thus, these combined effects of MYC overexpression and downregulation of miRNAs play a central regulatory role in the MYC oncogenic pathways and MYC-driven lymphomagenesis. Here, we provide biological insight on the function of MYC-regulated miRNAs, the mechanisms of MYC-induced miRNA repression, and the complicated feedback circuitry underlying lymphoma progression, as well as potential therapeutic targets in aggressive B-cell lymphomas.
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