Background
Non-small cell lung cancer (NSCLC) is one of the most common malignant tumors. The prognosis of patients with advanced NSCLC is poor due to metastasis. In recent years, the role of long non-coding RNAs (lncRNAs), a class of non-coding RNA molecules, in NSCLC has become an increasingly popular focus of studies. This study aimed to investigate the effects of ZNF674-AS1 and microRNA (miR)-23a on the migration and invasion abilities of NSCLC cells in vitro and explore the underpinning molecular mechanisms.
Conclusions
ZNF674-AS1 inhibits the migration and invasion of NSCLC cells by regulating a miR-23a/E-cadherin axis. ZNF674-AS1 and miR-23a could become potential therapeutic targets for NSCLC.
Methods
The expression levels of ZNF674-AS1 and miR-23a in NSCLC tissues and cells were detected by quantitative real-time polymerase chain reaction (qRT-PCR). Scratch test and transwell test were used to detect the effects of ZNF674-AS1 and miR-23a on the migration and invasion of NSCLC cells. The luciferase reporter gene experiment was used to verify miRNA targets. Western blot experiments were used to analyze protein expression.
Results
ZNF674-AS1 was downregulated in NSCLC tissues and cells, and inhibited the migration and invasion of NSCLC cells in vitro. In contrast, the expression of miR-23a, a downstream target of ZNF674-AS1, was increased in NSCLC tissues and cells. We found that miR-23a could antagonize the role of ZNF674-AS1 in NSCLC. E-cadherin was identified as a downstream target gene of miR-23a, and miR-23a could directly inhibit its expression. Conclusions: ZNF674-AS1 inhibits the migration and invasion of NSCLC cells by regulating a miR-23a/E-cadherin axis. ZNF674-AS1 and miR-23a could become potential therapeutic targets for NSCLC.