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. 2016 Jun 10;7(27):42566–42578. doi: 10.18632/oncotarget.9934

Figure 3. MicroR-135a-5p is critical for down-regulation of KLF4 by TGF-β1.

Figure 3

A. and B. HCC cells were transfected with 100nM miR-135a-5p mimic or 200nM inhibitor, immunoblot and qRT-PCR analysis of KLF4 was performed, data were presented as mean ± SEM (*,P<0.05; **, P<0.01, n=3). C. predicted sequences of the miR-135a-5p binding sites within the 3′-UTR of KLF4 and the luciferase reporter constructs containing KLF4 3′-UTR with either wild-type (WT) or mutant(MUT) miR-135a-5p target sites(left). Luciferase activity in Bel-7402 cell upon transfection of miR-135a-5p mimic or NC for 48h together with WT or MUT KLF4 3′-UTR luciferase reporter constructs(*,P<0.05). D. SK-Hep-1 and Bel-7402 cell were transfected with miR-135a-5p mimic or inhibitor or their controls for 24h, respectively, and were treated with or without 10ng/mL TGF-β1 for another 24h and then harvested. The mRNA level of KLF4 was examined by qRT-PCR and normalized to β-actin (*, P<0.01, n=3). E. HCC cells were transfected with 100nM miR-135a-5p mimic or 200nM inhibitor or their controls, qRT-PCR analysis of E-cadherin was performed (*,P<0.05; **, P<0.01, n=3).