The c‐Myc proto‐oncogene is activated in more than half of all human cancers. However, the precise regulation of c‐Myc protein stability is unknown. Here, we show that the lncRNA‐MIF (c‐Myc inhibitory factor), a c‐Myc‐induced long non‐coding RNA, is a competing endogenous RNA for miR‐586 and attenuates the inhibitory effect of miR‐586 on Fbxw7, an E3 ligase for c‐Myc, leading to increased Fbxw7 expression and subsequent c‐Myc degradation. Our data reveal the existence of a feedback loop between c‐Myc and lncRNA‐MIF, through which c‐Myc protein stability is finely controlled. Additionally, we show that the lncRNA‐MIF inhibits aerobic glycolysis and tumorigenesis by suppressing c‐Myc and miR‐586.
The lncRNA‐MIF, induced by c‐Myc, acts as a ceRNA to attenuate the inhibitory effect of miR‐586 on the E3 ligase Fbxw7 and thus inhibits aerobic glycolysis and tumorigenesis by promoting c‐Myc degradation.
c‐Myc transcriptionally activates the lncRNA‐MIF, which competes with the Fbxw7 mRNA for miR‐586.
A feedback loop exists between c‐Myc and lncRNA‐MIF, through which c‐Myc protein stability is finely controlled.
LncRNA‐MIF inhibits aerobic glycolysis and tumorigenesis.
- Received January 20, 2016.
- Revision received May 17, 2016.
- Accepted May 23, 2016.
- © 2016 The Authors