After the potential molecular targets of the miR-200 family were shown in the presentstudy, we sought to explore the effect of miR-200s on EMT in the metastatic NSCLC cells.Re-expression of miR-200c induced a 1.53-fold upregulation of E-cadherin(CDH1) through the downregulation of the E-cadherin repressortranscriptional factors ZEB1 and ZEB2, which isconsistent with previous studies in breast cancer or NSCLC cells (16,30,31)(Fig. 2B). The gene discussed is CDH1; the disease is breast carcinoma.