Copyright
©The Author(s) 2017.
World J Gastroenterol. Mar 14, 2017; 23(10): 1816-1827
Published online Mar 14, 2017. doi: 10.3748/wjg.v23.i10.1816
Published online Mar 14, 2017. doi: 10.3748/wjg.v23.i10.1816
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.
- Citation: Sun C, Wang FJ, Zhang HG, Xu XZ, Jia RC, Yao L, Qiao PF. miR-34a mediates oxaliplatin resistance of colorectal cancer cells by inhibiting macroautophagy via transforming growth factor-β/Smad4 pathway. World J Gastroenterol 2017; 23(10): 1816-1827
- URL: https://www.wjgnet.com/1007-9327/full/v23/i10/1816.htm
- DOI: https://dx.doi.org/10.3748/wjg.v23.i10.1816