| First Author | Glasgow SM | Year | 2013 |
| Journal | J Neurosci | Volume | 33 |
| Issue | 33 | Pages | 13560-8 |
| PubMed ID | 23946414 | Mgi Jnum | J:200897 |
| Mgi Id | MGI:5510248 | Doi | 10.1523/JNEUROSCI.0321-13.2013 |
| Citation | Glasgow SM, et al. (2013) The miR-223/Nuclear Factor I-A Axis Regulates Glial Precursor Proliferation and Tumorigenesis in the CNS. J Neurosci 33(33):13560-13568 |
| abstractText | Contemporary views of tumorigenesis regard its inception as a convergence of genetic mutation and developmental context. Glioma is the most common and deadly malignancy in the CNS; therefore, understanding how regulators of glial development contribute to its formation remains a key question. Previously we identified nuclear factor I-A (NFIA) as a key regulator of developmental gliogenesis, while miR-223 has been shown to repress NFIA expression in other systems. Using this relationship as a starting point, we found that miR-223 can suppress glial precursor proliferation via repression of NFIA during chick spinal cord development. This relationship is conserved in glioma, as miR-223 and NFIA expression is negatively correlated in human glioma tumors, and the miR-223/NFIA axis suppresses tumorigenesis in a human glioma cell line. Subsequent analysis of NFIA function revealed that it directly represses p21 and is required for tumorigenesis in a mouse neural stem cell model of glioma. These studies represent the first characterization of miR-223/NFIA axis function in glioma and demonstrate that it is a conserved proliferative mechanism across CNS development and tumorigenesis. |
