BACKGROUND Oral squamous cell carcinoma (OSCC) is a common malignancy in the oral and maxillofacial regions with an increasing incidence rate. Circular RNA (circRNA) is a recently discovered long-chain noncoding RNA family member. The objective of this study was to analyze the role of circ_0068162 in OSCC development. METHODS We downloaded sample data GSE145608 from the Gene Expression Omnibus database. Online databases starbase, TargetScan and miRDB were used to predict the target miRNAs and genes. Cell viability and proliferation were assessed using the CCK-8 and EdU assays, respectively. Cell migration and invasion abilities were detected using transwell assay. The double luciferase reporter and RIP assays were performed to verify the interaction relationship between the identified target molecules. RNase R and actinomycin D treatment were performed to analyze the stability of circ_0068162. RESULTS We found that circ_0068162 was overexpressed in the cytoplasm of OSCC cells and clinical OSCC tissues. Knockdown of circ_0068162 inhibited the growth, migration and invasion of OSCC cells. We also identified miR-186 as the target miRNA of circ_0068162, and JAG1 and JAG2 as the target genes of miR-186. The miR-186 inhibitor rescued the effects of sh-circ_0068162 and JAG1/JAG2 overexpression rescued the effects of miR-186 mimic in OSCC cells. Furthermore, ESRP1 promoted the biosynthesis of circ_0068162. CONCLUSION The circ_0068162/miR-186/JAGs/ESRP1 feedback loop is closely related to OSCC development.

中文翻译：

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源自 circ_0068162 的剪接因子 ESRP1 通过 miR-186/JAG 轴促进口腔鳞状细胞癌的进展。

背景口腔鳞状细胞癌（OSCC）是口腔颌面部常见的恶性肿瘤，发病率呈上升趋势。环状RNA（circRNA）是最近发现的长链非编码RNA家族成员。本研究的目的是分析 circ_0068162 在 OSCC 发展中的作用。方法 我们从 Gene Expression Omnibus 数据库下载了样本数据 GSE145608。使用在线数据库starbase、TargetScan和miRDB来预测目标miRNA和基因。分别使用 CCK-8 和 EdU 测定评估细胞活力和增殖。采用Transwell实验检测细胞迁移和侵袭能力。进行双荧光素酶报告基因和 RIP 测定以验证已识别的靶分子之间的相互作用关系。进行 RNase R 和放线菌素 D 处理以分析 circ_0068162 的稳定性。结果我们发现circ_0068162在OSCC细胞和临床OSCC组织的细胞质中过表达。circ_0068162的敲低抑制了OSCC细胞的生长、迁移和侵袭。我们还确定miR-186为circ_0068162的靶miRNA，JAG1和JAG2为miR-186的靶基因。在 OSCC 细胞中，miR-186 抑制剂挽救了 sh-circ_0068162 的作用，而 JAG1/JAG2 过表达则挽救了 miR-186 模拟物的作用。此外，ESRP1促进circ_0068162的生物合成。结论 circ_0068162/miR-186/JAGs/ESRP1反馈环与OSCC的发生密切相关。