Abstract

Background

Sinonasal squamous cell carcinoma (SNSCC) is a main subtype of sinonasal malignancy with unclear pathogenesis. microRNAs (miRNAs) are involved in SNSCC progression. Nevertheless, the role and mechanism of miR-362-3p in SNSCC development are unclear.

Methods

The SNSCC tissues (n = 23) and normal sinonasal samples (n = 13) were harvested. SNSCC cell line RPMI-2650 cells were transfected using Lipofectamine 3000. miR-362-3p and pituitary tumor-transforming gene 1 (PTTG1) were determined by quantitative reverse transcription polymerase chain reaction and western blot. Cell proliferation was analyzed via Cell Counting Kit-8 and 5-ethynyl-2′-deoxyuridine assays. Cell migration and invasion was assessed using wound healing assay and transwell assay. Epithelial-mesenchymal transition (EMT)-associated protein (E-cadherin, N-cadherin and Vimentin) levels were measured via western blot. The binding relationship was analyzed via bioinformatic analysis and dual-luciferase reporter assay.

Results

miR-362-3p abundance was decreased in SNSCC samples. miR-362-3p addition constrained cell proliferation, migration, invasion and EMT, but miR-362-3p knockdown played an opposite effect. PTTG1 was targeted and negatively modulated by miR-362-3p. PTTG1 abundance was elevated in SNSCC samples. PTTG1 overexpression mitigated miR-362-3p-modulated suppression of cell proliferation, migration, invasion and EMT in SNSCC cells.

Conclusion

miR-362-3p repressed cell proliferation, migration, invasion and EMT in SNSCC via targeting PTTG1.

中文翻译：

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miR-362-3p通过直接靶向垂体肿瘤转化基因1抑制鼻窦鳞状细胞癌进展

摘要

背景

鼻窦鳞状细胞癌（SNSCC）是鼻腔恶性肿瘤的主要亚型，发病机制尚不清楚。microRNA (miRNA) 参与 SNSCC 进展。然而，miR-362-3p 在 SNSCC 发展中的作用和机制尚不清楚。

方法

采集 SNSCC 组织 ( n  = 23) 和正常鼻腔样本 ( n  = 13)。使用 Lipofectamine 3000 转染 SNSCC 细胞系 RPMI-2650 细胞。通过定量逆转录聚合酶链反应和蛋白质印迹测定 miR-362-3p 和垂体肿瘤转化基因 1 (PTTG1)。通过Cell Counting Kit-8 和 5-ethynyl-2'-deoxyuridine 测定分析细胞增殖。使用伤口愈合测定和transwell测定评估细胞迁移和侵袭。通过蛋白质印迹测量上皮间质转化 (EMT) 相关蛋白 (E-钙粘蛋白、N-钙粘蛋白和波形蛋白) 水平。通过以下方式分析绑定关系生物信息学分析和双荧光素酶报告基因分析。

结果

SNSCC 样本中 miR-362-3p 丰度降低。添加 miR-362-3p 可抑制细胞增殖、迁移、侵袭和 EMT，但 miR-362-3p 敲低则起到相反的作用。PTTG1 被 miR-362-3p 靶向和负调控。SNSCC 样品中的 PTTG1 丰度升高。PTTG1 过表达减轻了 miR-362-3p 调节的 SNSCC 细胞中细胞增殖、迁移、侵袭和 EMT 的抑制。

结论

miR-362-3p通过靶向 PTTG1 抑制SNSCC 中的细胞增殖、迁移、侵袭和 EMT 。