Targeting lncRNA PSMA3-AS1, a Prognostic Marker, Suppresses Malignant Progression of Oral Squamous Cell Carcinoma

Abstract

Objective. Oral squamous cell carcinoma (OSCC) represents the most common maxillofacial malignancy. This study elucidated the clinicopathological value and molecular mechanisms of PSMA3 antisense RNA 1 (PSMA3-AS1) in OSCC. Methods. Totally, 135 OSCC patients were recruited. PSMA3-AS1 expression and its prognostic value were assessed in this cohort. si-PSMA3-AS1 was transfected into HN4 and CAL-27 OSCC cells. Then, cell proliferation was evaluated by CCK-8, colony formation, and EdU staining. Migration and invasion were investigated through wound healing, transwell, and western blot. The PSMA3-AS1/miR-136-5p and miR-136-5p/FN1 interactions were validated by dual luciferase report, real-time quantitative polymerase chain reaction (RT-qPCR), and western blot. Results. PSMA3-AS1 upregulation was determined in OSCC tissues. The upregulation indicated pessimistic patients’ outcomes. Multivariate Cox regression analyses confirmed PSMA3-AS1 as an independent prognostic indicator. Its upregulation was also found in OSCC cells. Under transfection with si-PSMA3-AS1, proliferation, migration, and invasion were all restrained in HN4 and CAL-27 OSCC cells. Furthermore, its knockdown induced the increase in E-cadherin expression and the reduction in N-cadherin and Vimentin expression. PSMA3-AS1 was a sponge of miR-136-5p. Mutual inhibition was found between two and the interactions were confirmed by dual luciferase report. It was confirmed that FN1 was a target of miR-136-5p. FN1 expression was increased by miR-136-5p inhibitors, which was lessened by si-PSMA3-AS1 cotransfection. Conclusion. Collectively, PSMA3-AS1 as a risk factor facilitated malignant behaviors of OSCC cells, related to the miR-136-5p/FN1 axis. Hence, PSMA3-AS1 as a potential therapeutic target for OSCC deserved further exploration.