ZEB1 and neoplasm: In NSCLCs, miR-200b and miR-200c, which are able to bind Zeb2 at positions 1015-1036 of its 3′-UTR, were up-regulated48, 49, and may therefore antagonize the effects of miR-144 on Zeb2. Hence, our results indicated that miR-144 is an important tumour suppressor that is inactivated during malignant transformation, and the miR-144-Zeb1 signal pathway could represent a rational therapeutic target.