Observed an inverse correlation between the expression of miR-138-5p and GPR124 in lung adenocarcinoma specimens. Knockdown of GPR124 mimicked the effects of miR-138-5p on the sensitivity to gefitinib.

our data demonstrate that the miR-138/SENP1 cascade is relative to radiosensitization in lung cancer cells and is a potential radiotherapy target.

Loss of MIRN138 expression is associated with non-small cell lung cancer.

MicroRNA-138 interacts with cyclin D3 and negatively regulates non-small cell lung cancer cells

In this paper, the authors found that miR-138 showed a pronounced increase after p53 activation in human non-small cell lung cancer (NSCLC) cells, which is mediated by p53 binding sites in the promoter region of its host gene, but this did not happen with rat and mouse cells.

miR-138 may play a suppressive role in the growth and metastasis of non small cell lung cancer cells partly at least by targeting YAP1

Therefore, miR-138/LIMK1/cofilin may be considered a potential therapeutic target for the treatment of non-small cell lung cancer

It may inhibit the proliferation, invasion and migration of lung cancer through downregulation of Sirt1 expression and activation of cell autophagy. The downregulation of miR-138 is closely related to the development of lung cancer

Low miR-138 expression is associated with Non-Small Cell lung cancer.

Low miR138 expression is associated with Nonsmall Cell lung cancer.

Taken together, these findings indicate TGFbeta1-induced down-regulation of microRNA-138 contributes to EMT in primary lung cancer cells, and suggest that miR-138 might serve as a potential therapeutic target.

MiR-138-5p inhibits epithelial-mesenchymal transition, growth and metastasis of lung adenocarcinoma cells through targeting ZEB2.