No abstract

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.

No abstract

No abstract

No abstract