Therefore, miR‑200b and miR‑200c targeted the expression of RhoE and inhibited the malignancy of NSCLC cells, and the downregulation of miR‑200b and miR‑200c may contribute to the high expression of RhoE in NSCLC.
The present findings suggest that miR-200c overexpression is significantly associated with poor survival rates in NSCLC and that miR-200c could play an oncogenic role. miR-200c may have clinical potential as a promising prognostic predictor for patients with NSCLC.
In another gefitinib-resistant NSCLC cell line (H1975 cells), similar to the findings in HCC827GR cells, both miR-155 and miR-200c were absent, and the EMT was induced along with epigenetic modifications.
The expression levels of miR‑200c were significantly reduced in NSCLC cell lines compared with in normal lung epithelial cells, as determined by reverse transcription‑quantitative polymerase chain reaction.
Overall, these findings indicated that miR-200c might be a predictive biomarker for sensitivity to EGFR-TKIs in advanced NSCLC patients with wild-type EGFR.
Compared with the benign control group, miR-126 expression was significantly downregulated in NSCLCs (p < 0.001), while miR-200c expression was significantly upregulated in NSCLCs (p < 0.001).
Further studies revealed that USP25 was a downstream target of miR-200c in NSCLC cells as miR-200c bound directly to the 3'-untranslated region of USP25, thus reducing both the messenger RNA and protein levels of USP25.
Finally, log-rank and Cox regression tests demonstrated that high expressions of tumor miR 21 and miR-200c or serum miR-21 were associated with a poor survival in NSCLC patients.
These data indicate that the loss of miR-200c expression induces an aggressive, invasive, and chemoresistant phenotype, and that assessment of its expression could contribute to a better clinicopathologic definition of patients with NSCLC.