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The miR-223/nuclear factor I-A axis regulates glial precursor proliferation and tumorigenesis in the CNS.
|Title||The miR-223/nuclear factor I-A axis regulates glial precursor proliferation and tumorigenesis in the CNS.|
|Publication Type||Journal Article|
|Year of Publication||2013|
|Authors||Glasgow SM, Laug D, Brawley VS, Zhang Z, Corder A, Yin Z, Wong STC, Li X-N, Foster AE, Ahmed N, Deneen B|
|Journal||The Journal of neuroscience : the official journal of the Society for Neuroscience|
|Date Published||2013 Aug 14|
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.
|Alternate Journal||J. Neurosci.|