MIR218-1 and MIR218-2 are deleted and downregulated in lung squamous cell carcinoma.

ADAM9 up-regulates N-cadherin via miR-218 suppression in lung adenocarcinoma cells.

MiR-205/miR-218 expression is associated with carboplatin chemoresistance and regulation of apoptosis via Mcl-1 and survivin signaling in lung cancer cells.

downregulation of miR-218 may contribute to the chemoresistance of non-small cell lung cancer cells to cisplatin, which leads to upregulation of RUNX2

the results of this study highlight an important role for miR-218-5p in the regulation of epidermal growth factor receptor in non-small cell lung cancer

Low miR218 expression is associated with cell migration and invasion in lung squamous cell carcinoma.

overexpression of miR-218 in H1299 increased chemosensitivity of cells to cisplatin treatment through suppression of Slug and ZEB2. These findings highlight an important role of miR-218 in the regulation of EMT-related traits and metastasis of lung cancer in part by modulation of Slug/ZEB2 signaling, and provide a potential therapeutic strategy by targeting miR-218 in lung cancer.

Studied the tumor suppressive role and antiproliferative effect of MicroRNA-218 in lung cancer cells through targeting of IL-6/STAT3 pathway.

miR-218-5p suppresses the killing effect of natural killer cells to lung adenocarcinoma cells by targeting SHMT1.

MicroRNA-218 regulates the epithelial-to-mesenchymal transition and the PI3K/Akt signaling pathway to suppress lung adenocarcinoma progression by directly targeting BMI-1.

Long noncoding RNA CCAT1 enhances human nonsmall cell lung cancer growth through downregulation of microRNA218.

Effects and mechanism of microRNA218 against lung cancer.