Abstract
The microRNA (miR)-200 family has been demonstrated to be associated with the tumorigenesis and progression of multiple types of human cancer, including non-small cell lung cancer (NSCLC). As a member of the miR-200 family, miR-429 was recently identified to have an oncogenic role in NSCLC. However, the role of miR-429 in NSCLC growth as well as the underlying mechanism remains to be fully elucidated. In the present study, NSCLC cell line H1229 was transfected with miR-429 mimic or inhibitor, respectively. It was observed that overexpression of miR-429 led to a significant increase in NSCLC cell proliferation, while knockdown of miR-429 suppressed the proliferation of H1229 cells. Bioinformatic prediction suggested that deleted in liver cancer 1 (DLC-1), a tumor suppressor in NSCLC, was a putative target gene of miR-429. Therefore, a luciferase reporter assay was performed and confirmed that miR-429 was able to bind the 3'-untranslated region of DLC-1 mRNA in H1229 cells. Furthermore, overexpression of miR-429 inhibited the protein expression of DLC-1, while knockdown of miR-429 promoted the protein expression of DLC-1 in NSCLC H1229 cells. In addition, overexpression of DLC-1 not only inhibited H1229 cell proliferation, but also additionally reversed the promoting effect of miR-429 overexpression on H1229 cell proliferation. Based on these findings, the present study suggests that miR-429 may have an oncogenic role in the regulation of cell proliferation via direct inhibition of DLC-1 protein expression in NSCLC cells. Therefore, miR-429 may present a putative therapeutic target for the treatment of NSCLC growth.