The loss of miR-200c expression induces an aggressive, invasive, and chemoresistant phenotype in non-small cell lung cancer.

High expression of serum MIR200C is associated with lung cancer.

Our results suggest that miR-126 might play tumor-suppressive and miR-200c an oncogenic role in non-small cell lung cancer

these findings indicated that miR-200c might be a predictive biomarker for sensitivity to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors in advanced non-small cell lung cancer patients with wild-type EGFR.

The miR-200c and the miR-183~96~182 cluster target Foxf2 to inhibit invasion and metastasis in lung cancers.

Low miR200c expression is associated with small cell lung cancer.

EMT was reversed by miR200c, which suggests that miR200c may serve a role in mediating the sensitivity of NCI2228/CRI cells to crizotinib. The present study may therefore contribute to improving the sensitivity of ALK positive lung cancer cells to crizotinib

The findings indicate that miR-200c fine-tuned the antioxidant response of the lung cancer cells to oxidative stress through several pathways.

In summary, our results demonstrated that miR-200c could suppress EMT, invasion, and migration of non-small cell lung cancer cells by downregulating HMGB1.

Low miR200c expression is associated with Non-Small Cell lung cancer.

miR200b and miR200c targeted the expression of RhoE and inhibited the malignancy of nonsmall cell lung cancer (NSCLC) cells, and the downregulation of miR200b and miR200c may contribute to the high expression of RhoE in NSCLC.

MiR-200c-3p suppression is associated with development of acquired resistance to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors in EGFR mutant non-small cell lung cancer via a mediating epithelial-to-mesenchymal transition (EMT) process.