Research Paper Volume 13, Issue 13 pp 17349—17369

miR-144-3p inhibited the growth, metastasis and epithelial-mesenchymal transition of colorectal adenocarcinoma by targeting ZEB1/2

miR-144-3p inhibited EMT process of CRA cells. (A) Representative images of cytoskeleton showed that miR-144-3p affected polymerization of F-actin and cellular morphology of CRA cells. (B) qRT-PCR analysis of the expression level of epithelial marker E-cadherin and mesenchymal marker vimentin in CRA cells. (C) Western blot analysis of the expression level of E-cadherin and vimentin in CRA cells. (D) Representative IF images showed the expression of E-cadherin and vimentin in CRA cells. (E) Flow cytometry analysis of E-cadherin and Vimentin in CRA cells. The results showed that E-cadherin expression was enriched and vimentin expression was reduced in Lovo cells treated with miR-144-3p mimic, while opposite results were observed in HCT116 cells treated with miR-144-3p inhibitor. ***, P

Figure 4. miR-144-3p inhibited EMT process of CRA cells. (A) Representative images of cytoskeleton showed that miR-144-3p affected polymerization of F-actin and cellular morphology of CRA cells. (B) qRT-PCR analysis of the expression level of epithelial marker E-cadherin and mesenchymal marker vimentin in CRA cells. (C) Western blot analysis of the expression level of E-cadherin and vimentin in CRA cells. (D) Representative IF images showed the expression of E-cadherin and vimentin in CRA cells. (E) Flow cytometry analysis of E-cadherin and Vimentin in CRA cells. The results showed that E-cadherin expression was enriched and vimentin expression was reduced in Lovo cells treated with miR-144-3p mimic, while opposite results were observed in HCT116 cells treated with miR-144-3p inhibitor. ***, P < 0.001.