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. 2017 Mar 14;23(10):1816–1827. doi: 10.3748/wjg.v23.i10.1816

Figure 3.

Figure 3

miR-34a directly regulated Smad4 expression and TGF-β inhibition in colorectal cancer cells. A: miRNA target prediction screened one computative miR-34a binding site at Smad4 3’-UTR; B: qRT-PCR analysis of expression of miR-34a treated with miR-34a mimics in HT29 and HT29-OXA cells (aP < 0.05). U6 was used as a loading control. Error bars represent mean ± SD from three independent experiments; C: 3’-UTR luciferase reporter assay showed a reduction of relative luciferase activity of wild-type Smad4 3’-UTR by pre-miR-34a in HT29 and HT29-OXA cells (eP < 0.001); D: Western blotting of Smad4 and TGF-β expression in HT29 and HT29-OXA cells treated with miR-34a mimic. β-actin expression level was used as internal loading control.