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. Author manuscript; available in PMC: 2021 Apr 15.
Published in final edited form as: J Am Chem Soc. 2020 Apr 1;142(15):6970–6982. doi: 10.1021/jacs.9b13159

Figure 1.

Figure 1.

Schematic of the pri-miR-17–92 cluster and its downstream targets. (A) Schematic of the polycistronic pri-miR-17–92 cluster’s secondary structure. Interestingly, miR-17, miR-18a, and miR-20a share a common structure at their Dicer sites, the 1-nucleotide bulge 5′G_U/3′CUA targetable with 1 (yellow boxes). Adjacent targetable motifs are present in all three miRNAs, 5′GGU/3′C_A in miR-17 and miR-20a (blue box) and 5′GAU/3′C_A in miR-18a (green box). (B) In DU-145 prostate cancer cells, miR-18a represses STK4, which inhibits apoptosis. (C) In triple negative breast cancer cells, overexpression of miR-17 and miR-20a induces an invasive phenotype. (D) In polycystic kidney disease, miR-17, miR-19a, and miR-19b are upregulated, triggering cell proliferation and cyst formation.