Abstract
Of critical importance in the stress response is the post-transcriptional control of the expression of important genes involved in the control of cell survival and apoptosis. Here we report that miR-19, an oncogenic component of the miR-17-92/Oncomir-1 microRNA polycistron, regulates the expression of Ras homolog B (RhoB) in keratinocytes upon exposure to ultraviolet (UV) radiation. Strikingly, we could not find any evidence for deregulated expression of miR-19 during UV treatment. However, we show that miR-19-mediated regulation of antiapoptotic RhoB expression requires the binding of human antigen R (HuR), an AU-rich element binding protein, to the 3′-untranslated region of the rhoB mRNA. We propose that the loss of the interdependent binding between HuR and miR-19 to the rhoB mRNA upon UV exposure relieves this mRNA from miR-19-dependent inhibition of translation and contributes to the apoptotic response.
| Original language | English |
|---|---|
| Pages (from-to) | 1692-1701 |
| Number of pages | 10 |
| Journal | Cell Death and Differentiation |
| Volume | 18 |
| Issue number | 11 |
| DOIs | |
| Publication status | Published - 1 Jan 2011 |
| Externally published | Yes |
Keywords
- Rho GTPase
- apoptosis
- mRNA binding protein
- mRNA translation
- microRNA