In conclusion, the results of this study demonstrate that URGCP increases transcription factor c-myc expression through activating the classical NF-κB pathway in glioma; Transcription factor c-myc suppresses miR-16 expression through binding to the promoter of miR-16; Cyclin D1 and Cyclin E1 are indentified as the direct targets of miR-16, thus, low-levels of miR-16 leads to G1/S phase transition and tumor growth by enhancing the expression of Cyclin D1 and Cyclin E1 in vivo and in vitro (Fig. 6). Here, NFKB1 is linked to glioma.