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Background  Inflammatory cytokines and transforming growth factor-β (TGF-β) are mutually inhibitory. However, hyperactivation of nuclear factor-κB (NF-κB) and TGF-β signaling both emerge in glioblastoma. Here, we report microRNA-148a (miR-148a) overexpression in glioblastoma and that miR-148a directly suppressed Quaking (QKI), a negative regulator of TGF-β signaling.    Methods  We determined NF-κB and TGF-β/Smad signaling activity using pNF-κB-luc, pSMAD-luc, and control plasmids. The association between an RNA-induced silencing complex and  QKI , mitogen-inducible gene 6 ( MIG6 ), S-phase kinase–associated protein 1 ( SKP1 ), and glyceraldehyde-3-phosphate dehydrogenase ( GAPDH ) mRNA was tested with microribonucleoprotein immunoprecipitation and real-time PCR. Xenograft tumors were established in the brains of nude mice.    Results  QKI suppression induced an aggressive phenotype of glioblastoma cells both  in vitro  and  in vivo . Interestingly, we found that NF-κB induced miR-148a expression, leading to enhanced-strength and prolonged-duration TGF-β/Smad signaling. Notably, these findings were consistent with the significant correlation between miR-148a levels with NF-κB hyperactivation and activated TGF-β/Smad signaling in a cohort of human glioblastoma specimens.    Conclusions  These findings uncover a plausible mechanism for NF-κB–sustained TGF-β/Smad activation via miR-148a in glioblastoma, and may suggest a new target for clinical intervention in human cancer.    Electronic supplementary material  The online version of this article (doi:10.1186/1476-4598-14-2) contains supplementary material, which is available to authorized users.

NF-κB induces miR-148a to sustain TGF-β/Smad signaling activation in glioblastoma