Long noncoding RNA PSMA3‑AS1 functions as a microRNA‑409‑3p sponge to promote the progression of non‑small cell lung carcinoma by targeting spindlin 1.

Abstract

PSMA3 antisense RNA 1 (PSMA3-AS1), a long noncoding RNA, promotes the progression of esophageal squamous cell carcinoma. However, no study to date has explored the expression or roles of PSMA3-AS1 in non-small cell lung carcinoma (NSCLC). The present study examined the expression profile and role of PSMA3-AS1 in NSCLC. It also aimed to identify how PSMA3-AS1 promotes the malignant phenotype of NSCLC cells. PSMA3-AS1 expression in NSCLC tissues and cell lines was measured by reverse transcription-quantitative polymerase chain reaction. Cell Counting Kit-8, cell apoptosis, Transwell migration and invasion, and xenograft tumor assays were conducted to study the effects of PSMA3-AS1 on the aggressive phenotype of NSCLC cells. Furthermore, bioinformatics analysis, RNA immunoprecipitation, luciferase reporter assay, western blotting, and rescue experiments were used to elucidate the interaction among PSMA3-AS1, microRNA-409-3p (miR-409-3p), and spindlin 1 (SPIN1) in NSCLC cells. In the present study, high levels of PSMA3-AS1 were confirmed in both NSCLC tissues and cell lines. An increased PSMA3-AS1 level was correlated with advanced tumor-node-metastasis stage and increased lymph node metastasis. Patients with NSCLC with high PSMA3-AS1 levels had shorter overall survival than those with low PSMA3-AS1 levels. PSMA3-AS1 depletion significantly decreased NSCLC cell proliferation, migration, and invasion, as well as substantially increased cell apoptosis in vitro. Furthermore, PSMA3-AS1 deficiency decreased NSCLC tumor growth in vivo. Through molecular mechanism assays, it was revealed that PSMA3-AS1 acted as a molecular sponge for miR-409-3p and consequently increased SPIN1 expression. Notably, rescue experiments revealed that the inhibition of miR-409-3p or restoration of SPIN1 expression abrogated the effects of PSMA3-AS1 knockdown in NSCLC cells. Collectively, PSMA3-AS1 functioned as an oncogenic long noncoding RNA in NSCLC. PSMA3-AS1 sponged miR-409-3p and thus increased SPIN1 expression, promoting the aggressive phenotype of NSCLC cells.