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. 2016 Jun 7;7(29):45199–45213. doi: 10.18632/oncotarget.9900

Figure 5. miR-20a-5p promoted the onco-process of CRC cells via Smad4 repression.

Figure 5

miR-20a-5p overexpressing and negative control HT29 cells were transfected with empty vectors or Lv-Smad4. miR-20a-5p knocking down and negative control HCT-116 cells were transfected with empty vectors or shSmad4. (A) Wound healing assay, migration and invasion assays were performed in HT29 cells. Smad4 overexpression partially abrogated the increased wound healing, invasion and metastasis capacity induced by upregulation of miR-20a-5p. (B) Wound healing assay, migration and invasion assays were performed in HCT116 cells. Smad4 knockdown partially restored the decreased wound healing, invasion and metastasis capacity induced by downregulation of miR-20a-5p. (C) The expression level of E-cadherin and N-cadherin mRNA was evaluated by qRT-PCR. Overexpression or knockdown of Smad4 partially reversed the promoted or inhibited EMT due to miR-20a-5p upregulation or downregulation. (D) The expression level of E-cadherin and N-cadherin protein was evaluated by western blot analysis. (E) The number of tumor colonies formed in animal models. Overexpression or knockdown of Smad4 partially reversed the number of liver metastatic colonies resulting from miR-20a-5p upregulation or downregulation. (*P < 0.05; **P < 0.01, ***P < 0.001).