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. Author manuscript; available in PMC: 2020 Apr 15.
Published in final edited form as: Cancer Res. 2019 Aug 15;79(20):5151–5158. doi: 10.1158/0008-5472.CAN-18-3544

Figure 3. QKI-5 is a direct molecular target of miR-221.

Figure 3.

(A) Schematic representation of the predicted miR-221 target recognition sequence within the 3’UTR of the QKI-5 mRNA, and of the two mutations introduced to functionally disable it. Numbers correspond to nucleotide positions in QKI-5 sequence (GenBank: NM_001301085). (B) Suppression of the luciferase activity of pGL3 constructs encoding the WT version of the QKI-5 3’UTR, but not that encoding mutant QKI-5 3’UTR by miR-221 (n=3; *p<0.05, ***p<0.005). (C) Forced expression of miR-221 down-regulated endogenous QKI-5 protein levels in human HCT116 cells, while forced expression of an anti-miR-221 construct up-regulated them. Expression of β-actin was used as a control. (D) QKI and miR-221 expression levels are inversely correlated (r=−0.16, p<0.001) in the TCGA COAD database of human primary CRCs (n=439).