Long non‑coding RNA00887 reduces the invasion and metastasis of non‑small cell lung cancer by causing the degradation of miRNAs.

Abstract

Long non‑coding RNAs (lncRNAs) can act as carcinogenic or cancer suppressive factors during the pathogenesis, invasion and metastasis of non‑small cell lung cancer (NSCLC). The current study explored the role of long intergenic non‑protein coding RNA 00887 (LINC00887) and competing endogenous RNAs (ceRNAs). It was revealed that LINC00887 interacts with several microRNAs (miRs), which regulates downstream genes such as fibronectin1, MET proto‑oncogene, receptor tyrosine kinase and mothers against decapentaplegic homolog 4, which are associated with the spread of lung cancer. The experimental results also suggested that LINC00887 can stimulate miR‑613, miR‑206 and miR‑1‑2 to become competing endogenous RNAs, which may regulate the epithelial‑mesenchymal transition of NSCLC cells through the transforming growth factor‑â signal transduction pathway, and therefore promote the migration of cells and the acquisition of stem cell characteristics. Therefore, it can be concluded that high levels of LINC00887 can accelerate the malignant transformation ability of NSCLC cells.