Long non-coding RNA PITPNA-AS1 silencing suppresses proliferation, metastasis and epithelial-mesenchymal transition in non-small cell lung cancer cells by targeting microRNA-32-5p

Lung cancer is one of the most common types of cancer and has a high mortality rate, worldwide. The major histopathological subtype is non-small cell lung cancer (NSCLC). The aim of the present study was to investigate the role of long non-coding (lnc) RNA PITPNA antisense RNA 1 (PITPNA-AS1) in NSCLC and elucidate its potential mechanisms. The expression of PITPNA-AS1 was determined in several NSCLC cell lines. Following PITPNA-AS1-silencing, cell proliferation, invasion and migration were evaluated using Cell Counting Kit-8, colony formation, Transwell assay and wound healing assays, respectively. The expression levels of proliferation-, migration- and epithelial-mesenchymal transition (EMT)-associated proteins were examined using immunofluorescence assay or western blot analysis. A luciferase reporter assay was conducted to verify the potential interaction between PITPNA-AS1 and microRNA(miR)-32-5p. Subsequently, rescue assays were performed to investigate the effects of PITPNA-AS1 and miR-32-5p on NSCLC progression. The results demonstrated that PITPNA-AS1 was highly expressed in NSCLC tissues and cell lines. It was found that PITPNA-AS1 silencing inhibited the proliferation, invasion and migration of NSCLC cells. Furthermore, the protein expression of E-cadherin was upregulated, while the expression levels N-cadherin and vimentin were downregulated. The luciferase reporter assay confirmed that miR-32-5p was a direct target of PITPNA-AS1. The rescue experiments suggested that a miR-32-5p inhibitor significantly reversed the inhibitory effects of PITPNA-AS1 silencing on proliferation, invasion, migration and EMT in NSCLC cells. Collectively, the present results demonstrated that PITPNA-AS1 silencing could suppress the progression of NSCLC by targeting miR-32-5p, suggesting a promising biomarker in NSCLC diagnosis and treatment.