Zhang et al Dev Biol. 2007 Feb 1;302(1):1-12

Modulation of cell cycle transcription factor E2F1 by a c-Myc-regulated microRNA polycistron miR-17–92 and its function in cancer pathogenesis (O'Donnell et al., 2005). The upper part of the panel shows the schematic representation of the microRNA polycistron miR-17–92 cluster. The larger boxes represent the miRNA precursors (pre-miRNAs), and the smaller boxes within represent the mature miRNAs. c-Myc promotes the transcription of both miR-17–92 and E2F1 by binding at the CACGTG or CARGTG sites on the miR-17–92 gene (O'Donnell et al., 2005) and promoter sites of E2F1. Both miR-17-5p and miR-20a negatively regulate E2F1 gene expression through translational repression by directly binding miR-17-5p and miR-20a at the 3′UTR of E2F1 mRNAs. Level expression results in the inhibition of apoptosis through the ARF-p53 pathway, and causes cancer pathogenesis in several organs, including lung cancer and lymphomas. In this regulatory mechanism, miR-17–92 functions as an oncogene.