In summary, our results showed that SM-inhibited NSCLC cell growth through the reciprocal interaction between HOTAIR and miR-214-3p, which ultimately suppressed PDPK1 gene expression.
In the present study, the biological functions and potential mechanisms of miR‑214 were determined, as well as its correlation with HIF‑1α signaling in non‑small cell lung cancer (NSCLC) cells.
Results showed that miR-214 levels were significantly increased in the 7 NSCLC cell lines compared with those in the human bronchial epithelial cell line.
The results of the present study demonstrate that down-regulation of miR-214 may reverse acquired resistance to erlotinib in NSCLC through mediating its direct target gene LHX6 expression.
Sulforaphane inhibits cancer stem-like cell properties and cisplatin resistance through miR-214-mediated downregulation of c-MYC in non-small cell lung cancer.
We showed that downregulation of miRNA-214 increased invasive potential, and conversely, overexpression of miRNA-214 decreased invasiveness of NSCLC cells in vitro.