This study identified both PTTG1 and miR-186 as potential anti-invasion targets for therapeutic intervention in non-small cell lung cancer .

Data indicate that Rho-associated protein kinase 1 (ROCK1) was inversely correlated with miR-186 expression in non-small cell lung cancer (NSCLC).

Study found miR-186 expression significantly decreased in lung cancer tissues and cells and MAP3K2 expression increased in the same cancer tissues. Also, results confirmed that MAP3K2 is a target gene of miR-186 and both expression correlated with prognosis.

Study shows that miR186 is down-regulated in non-small cell lung cancer (NSCLC) tissues and reduces invasion ability of NSCLC cell lines by directly targeting cdc42 and modulating epithelial-mesenchymal transition process which effects cell adhesion. According to these findings, miR-186 is proposed to be one of the tumor-suppressors for NSCLC.

MiR-186-5p overexpression blocked the oncogenic effects of XIST on cell proliferation and invasion, suggesting that the effects of XIST on non-small cell lung cancer growth and invasion are partially mediated by miR-186-5p.

miR-186-5p expression was significantly up-regulated in LUAD tumor tissues and LUAD cell lines as compared with tumor-adjacent tissues and normal human lung epithelial cells, respectively. MiR-186-5p overexpression remarkably promoted the proliferation, migration and invasion of LUAD cells. This study demonstrated that miR-186-5p promotes the proliferation, migration and invasion of LUAD cells by targeting PTEN.

Upregulation of miR-186-5p suppresses cisplatin resistance in DDP resistant non-small-cell lung cancer cells both in vitro and in vivo, presumably by targeting SIX1.