We present for the first time evidence that miR-196a could directly interact with IkBa 3′-UTR to suppress IkBa expression and subsequently promote activation of NF-kB, consequently promoting proliferation of and suppressing apoptosis in GBM cells both in vitro and in vivo. Our study confirmed that miR-196a was upregulated in GBM specimens and that high levels of miR-196a were significantly correlated with poor outcome in a large cohort of GBM patients.
NSDNA: The Nervous System Disease NcRNAome Atlas
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