MicroRNA-206 inhibits the viability and migration of human lung adenocarcinoma cells partly by targeting MET

Abstract

Abstract. MicroRNA (miRNA)-based targeting in cancer has emerged as a potential therapeutic strategy. miR-206 has recently been implicated in cancer. However, the role and molecular mechanism of miR-206 in lung adenocarcinoma are still unclear. The present study revealed that miR-206 was downregulated in human lung adenocarcinoma tissues. Overexpression of miR-206 in human lung adenocarcinoma-derived cells significantly inhibited cell viability and migration. Further experiments indicated that the overexpression of miR-206 decreased the expression of MET at the messenger RNA and protein levels via direct targeting of MET in a 3'-untranslated region-dependent manner. The knockdown of MET by small interfering RNA partly led to a phenocopy effect of miR-206. In conclusion, the present study identified miR-206 as a potential tumor suppressor of lung adenocarcinoma that exerts its functions, in part, by negative regulation of MET.

miR‐1‐3p and miR‐206 sensitizes HGF‐induced gefitinib‐resistant human lung cancer cells through inhibition of c‐Met signalling and EMT

“…From our results and others, we can find that c‐Met targeting is the common character in these studies, although the experiments were conducted under different gefitinib‐resistant conditions. Previous studies showed that miR‐206 target c‐Met directly in lung cancer cells . In our study, we further demonstrated that both miR‐1‐3p and miR‐206 have common target c‐Met in EGFR mutant PC‐9 and HCC‐827 cells.…”

“…Previous studies showed that miR-206 target c-Met directly in lung cancer cells. 44 In our study, we further demonstrated that both miR-1-3p and miR-206 have common Epithelial-mesenchymal transition is another mechanism of acquired EGFR-TKI resistance in lung cancers. In vitro studies showed that the mesenchymal phenotype is more resistant to EGF-TKI than the epithelial phenotype.…”

Effects of MicroRNA-206 on Osteosarcoma Cell Proliferation, Apoptosis, Migration and Invasion by Targeting ANXA2 Through the AKT Signaling Pathway

“…Wang, et al also revealed that miR-206 overexpression promoted neural cell apoptosis by regulating Otx2, one of its target genes [27]. Furthermore, cell migration is a crucial step in cancer metastasis, and a previous study revealed that upregulation of miR-206 in lung adenocarcinoma cells inhibits cell migration [28]. In line with our results, another study also demonstrated that miR-206 might play a key role in the pathogenesis and development of OS and may provide a potential target for gene therapy [9].…”

microRNA-605 promotes cell proliferation, migration and invasion in non-small cell lung cancer by directly targeting LATS2

“…miRNAs negatively modulate gene expression through binding to the 3'-untranslated regions (3'UTRs) of the target genes in base pairing manner and therefore resulting in either translation suppression or corresponding mRNAs degradation (12). Accumulated studies have reported that miRNAs regulate approximately one third to as many as two thirds of human genes and are involved in a number of cellular biological processes, such as cell proliferation, apoptosis, metabolism, immunity and metastasis (13)(14)(15). To date, multiple miRNAs have been found to be abnormally expressed in NSCLC, such as miR-124 (16), miR-154 (17), miR-320 (18), miR-485 (19) and so on.…”