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. Author manuscript; available in PMC: 2013 Sep 21.
Published in final edited form as: Oncogene. 2012 May 14;32(12):1570–1579. doi: 10.1038/onc.2012.167

Figure 1. Rab1B is the direct target of miR502.

Figure 1

(A) A putative miR-502 binding site exists in the 3’-UTR of Rab1B mRNA and two point mutations were generated in the binding site. Ectopic expression of miR-502 or siRNAs against Rab1B (siRab1B) in HCT116 and SW480 cells decreased Rab1B protein levels by (B) Western blot analysis and (C) mRNA level by real-time qRT-PCR. (D) Transfection of miR-502 inhibited firefly luciferase activity of pMIR-REPORT-3UTRRab1B (wt) and such inhibition was absent with mutations in the miR-502 binding site (mut). The negative miRNA was used as the negative control in all experiments. The impact of miR-502 and siRab1B on Rab1B expression was normalized and compared to those of negative miRNA (n=3, p < 0.001).

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