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
- Lingling Wang
- Lei Wu
- Jinfeng Pang
Affiliations: Precision Medical Center, Affiliated Hospital of Beihua University, Jilin, Jilin 132011, P.R. China, Department of Thoracic Surgery, Jilin City Central Hospital, Capital Medical University, Jilin, Jilin 132010, P.R. China, Department of Neurosurgery, Affiliated Hospital of Beihua University, Jilin, Jilin 132011, P.R. China
- Published online on: July 15, 2020 https://doi.org/10.3892/or.2020.7693
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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.