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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的进展。

miR-362-3p suppresses sinonasal squamous cell carcinoma progression via directly targeting pituitary tumor-transforming gene 1.

机构信息

Department of E. N. T, Qingdao Jiaozhou Center Hospital, Qingdao, Shandong, China.

Department of Otolaryngology, Zibo Center Hospital, Zibo, Shandong, China.

出版信息

J Recept Signal Transduct Res. 2022 Feb;42(1):43-51. doi: 10.1080/10799893.2020.1839766. Epub 2020 Nov 4.

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 ( = 23) and normal sinonasal samples ( = 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 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 western blot. The binding relationship was analyzed 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 targeting PTTG1.

摘要

背景

鼻窦鳞状细胞癌(SNSCC)是一种主要的鼻窦恶性肿瘤亚型,其发病机制尚不清楚。microRNAs(miRNAs)参与了 SNSCC 的进展。然而,miR-362-3p 在 SNSCC 发展中的作用和机制尚不清楚。

方法

采集 23 例 SNSCC 组织和 13 例正常鼻窦样本。使用 Lipofectamine 3000 转染 SNSCC 细胞系 RPMI-2650 细胞。采用定量逆转录聚合酶链反应和 Western blot 检测 miR-362-3p 和垂体肿瘤转化基因 1(PTTG1)。采用细胞计数试剂盒-8 和 5-乙炔基-2'-脱氧尿苷测定法分析细胞增殖。采用划痕愈合试验和 Transwell 试验评估细胞迁移和侵袭。采用 Western blot 检测上皮-间充质转化(EMT)相关蛋白(E-钙黏蛋白、N-钙黏蛋白和波形蛋白)水平。通过生物信息学分析和双荧光素酶报告基因实验分析结合关系。

结果

miR-362-3p 在 SNSCC 样本中的丰度降低。miR-362-3p 的添加抑制了细胞增殖、迁移、侵袭和 EMT,但 miR-362-3p 的敲低则起到了相反的作用。PTTG1 是 miR-362-3p 的靶基因,并受到 miR-362-3p 的负调控。PTTG1 在 SNSCC 样本中的丰度升高。PTTG1 的过表达减轻了 SNSCC 细胞中 miR-362-3p 调节的细胞增殖、迁移、侵袭和 EMT 的抑制作用。

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。

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