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. 2013 Aug 6;4(9):1388–1398. doi: 10.18632/oncotarget.1239

Figure 3. miR-27a* coordinately downregulates the EGFR signaling axis via independent direct interactions with EGFR, AKT1, and mTOR.

Figure 3

(A) Further in silico screening of downstream members of the EGFR signaling axis, identified 5 putative binding sites for miR-27a* (black bars) on AKT1 and 11 binding sites for miR-27a* on mTOR; (B) Immunoblot shows decreased EGFR expression after the transfection of miR-27a*, −27a and −7 precursors. Downstream AKT1 and mTOR are also decreased when transfected with miR-27a*, but not miR-27a or −7; (C) Densitometry analysis quantifies the differences observed in the immunoblots, *p<0.01; (D) Detailed map of reporter plasmid constructs depicting the EGFR sequence placed downstream of luciferase in pGL3; (E) Luciferase assay after transfection of EGFR reporter plasmids and miR-27a* in HNSCC cells demonstrates E2145-pGL3 and E3908-pGL3 have functional binding sites for miR-27a* and that E160-pGL3 is a non-functional site, *p<0.05 and **p<0.005; (F) Luciferase assay after transfection of AKT1 and mTOR reporter plasmids plus miR-27a* in HNSCC cells demonstrates the 3'UTR of both signaling mediators have functional binding sites for miR-27a*, *p<0.001.