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miR-17-92 explains MYC oncogene addiction.
Yulin Li1, Stephanie C Casey1, Peter S Choi1
1Division of Oncology; Departments of Medicine and Pathology; Stanford University ; Stanford, CA USA.
Molecular & Cellular Oncology
|June 17, 2016
Summary
MYC oncogene addiction in cancer may stem from its regulation of the miR-17-92 microRNA cluster. This cluster influences critical cell fate decisions, including survival, death, self-renewal, and senescence.
Area of Science:
- Oncology
- Molecular Biology
- Gene Regulation
Background:
- The MYC oncogene is a key regulator of tumorigenesis, controlling the expression of numerous genes.
- MYC's role in cancer development is well-established, but its precise downstream effectors are still being elucidated.
Purpose of the Study:
- To investigate the role of the microRNA miR-17-92 cluster in mediating MYC's functions.
- To determine if addiction to MYC in cancer is linked to dependence on the miR-17-92 cluster.
Main Methods:
- Analysis of gene expression patterns regulated by MYC.
- Investigating the functional link between MYC and the miR-17-92 microRNA cluster.
Main Results:
- MYC regulates the miR-17-92 microRNA cluster.
- The miR-17-92 cluster mediates MYC's control over cell survival versus death decisions.
- The miR-17-92 cluster also regulates cell self-renewal versus senescence pathways.
Conclusions:
- MYC's oncogenic functions, including promoting tumorigenesis, are partly mediated by the miR-17-92 cluster.
- Cancer cell dependence on MYC may represent an addiction to the downstream miR-17-92 microRNA cluster.
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