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。

IF 2.6 4区 生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY
Zhaolun Meng, Shu Zhu, Na Liu, Jie Tian
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引用次数: 4

摘要

背景:鼻窦鳞状细胞癌(SNSCC)是鼻窦恶性肿瘤的主要亚型,发病机制尚不清楚。microRNAs (miRNAs)参与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:采集鼻窦鳞状细胞癌组织(n = 23)和正常鼻窦标本(n = 13)。用Lipofectamine 3000转染SNSCC细胞系rmi -2650细胞。采用定量逆转录聚合酶链反应和western blot检测miR-362-3p和垂体瘤转化基因1 (PTTG1)水平。通过细胞计数试剂盒-8和5-乙基-2'-脱氧尿苷法分析细胞增殖情况。采用伤口愈合试验和transwell试验评估细胞迁移和侵袭。western blot检测上皮-间质转化(EMT)相关蛋白(E-cadherin、N-cadherin和Vimentin)水平。结合关系通过生物信息学分析和双荧光素酶报告试验进行分析。结果:SNSCC样品中miR-362-3p丰度降低。添加miR-362-3p抑制细胞增殖、迁移、侵袭和EMT,而敲低miR-362-3p则起到相反的作用。PTTG1被miR-362-3p靶向并负向调节。PTTG1丰度在SNSCC样品中升高。PTTG1过表达减轻了mir -362-3p调节的SNSCC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细胞的增殖、迁移、侵袭和EMT。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
miR-362-3p suppresses sinonasal squamous cell carcinoma progression via directly targeting pituitary tumor-transforming gene 1.

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.

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来源期刊
Journal of Receptors and Signal Transduction
Journal of Receptors and Signal Transduction 生物-生化与分子生物学
CiteScore
6.60
自引率
0.00%
发文量
19
审稿时长
>12 weeks
期刊介绍: Journal of Receptors and Signal Tranduction is included in the following abstracting and indexing services: BIOBASE; Biochemistry and Biophysics Citation Index; Biological Abstracts; BIOSIS Full Coverage Shared; BIOSIS Previews; Biotechnology Abstracts; Current Contents/Life Sciences; Derwent Chimera; Derwent Drug File; EMBASE; EMBIOLOGY; Journal Citation Reports/ Science Edition; PubMed/MedLine; Science Citation Index; SciSearch; SCOPUS; SIIC.
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