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.

中文翻译：

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靶向 lncRNA PSMA3-AS1，一种预后标志物，抑制口腔鳞状细胞癌的恶性进展

客观。口腔鳞状细胞癌 (OSCC) 是最常见的颌面部恶性肿瘤。本研究阐明了 PSMA3 反义 RNA 1 (PSMA3-AS1) 在 OSCC 中的临床病理价值和分子机制。方法。总共招募了 135 名 OSCC 患者。在该队列中评估了 PSMA3-AS1 表达及其预后价值。将 si-PSMA3-AS1 转染到 HN4 和 CAL-27 OSCC 细胞中。然后，通过 CCK-8、集落形成和 EdU 染色评估细胞增殖。通过伤口愈合、transwell 和蛋白质印迹研究迁移和侵袭。通过双荧光素酶报告、实时定量聚合酶链反应 (RT-qPCR) 和蛋白质印迹验证 PSMA3-AS1/miR-136-5p 和 miR-136-5p/FN1 相互作用。结果. 在 OSCC 组织中测定了 PSMA3-AS1 上调。上调表明患者的结果悲观。多变量 Cox 回归分析证实 PSMA3-AS1 是一个独立的预后指标。在 OSCC 细胞中也发现了它的上调。转染si-PSMA3-AS1后，HN4和CAL-27 OSCC细胞的增殖、迁移和侵袭均受到抑制。此外，它的敲低诱导了 E-cadherin 表达的增加和 N-cadherin 和 Vimentin 表达的减少。PSMA3-AS1 是 miR-136-5p 的海绵。在两者之间发现了相互抑制，并且通过双荧光素酶报告证实了相互作用。证实FN1是miR-136-5p的靶标。miR-136-5p 抑制剂增加了 FN1 表达，而 si-PSMA3-AS1 共转染降低了 FN1 表达。结论. 总的来说，PSMA3-AS1 作为危险因素促进了 OSCC 细胞的恶性行为，与 miR-136-5p/FN1 轴相关。因此，PSMA3-AS1 作为 OSCC 的潜在治疗靶点值得进一步探索。