miR-362-3p 通过靶向调控垂体肿瘤转化基因 1 抑制口腔鳞状细胞癌细胞的侵袭和转移。

Xiao Ding, Jiawen Chen, Pengyu Qu, Chenyu Sun, Hongli Li, Wenting Hu, Xin Fan
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引用次数: 0

摘要

研究目的本研究旨在探讨垂体肿瘤转化基因 1(PTT-G1)在 miR-362-3p 作用下对口腔鳞状细胞癌(OSCC)细胞株侵袭和增殖的影响:方法:利用生物信息学在线数据库查询PTTG1在头颈部鳞状细胞癌(HNSCC)中的表达情况。通过 Western 印迹法检测了 PTTG1 在 Cal-27、HN-30 和 HOK 细胞系中的表达。伤口愈合试验用于确定 PTTG1 对 OSCC 细胞迁移能力的影响。Transwell试验用于检测细胞侵袭能力的变化。5-乙炔基-2'-脱氧尿苷(EdU)细胞增殖试验用于检测细胞增殖能力的变化。生物信息学方法预测了 PTTG1 的上游 miRNA。通过双荧光素酶试验检测了miR-362-3p与PTTG1之间的靶向关系,并采用实时定量聚合酶链反应(qRT-PCR)测定了miRNA在OSCC组织中的表达:结果:ENCORI数据库显示,PTTG1在OSCC组织中表达上调。Western印迹证实,与HOK细胞相比,PTTG1在Cal-27和HN-30细胞中表达上调。PTTG1敲除可抑制Cal-27和HN-30细胞的迁移、侵袭和增殖(研究结论:miR-362-3p可通过靶向PTTG1抑制Cal-27和HN-30细胞的侵袭和增殖。
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miR-362-3p inhibited the invasion and metastasis of oral squamous cell carcinoma cells by targeting the regulation of pituitary tumor-transforming gene 1.

Objectives: This study aimed to explore the effect of pituitary tumor-transforming gene 1 (PTT-G1) on the invasion and proliferation of oral squamous cell carcinoma (OSCC) cell lines under the action of miR-362-3p.

Methods: The bioinformatics online database was used to query the expression of PTTG1 in head and neck squamous cell carcinoma (HNSCC). The expression of PTTG1 in the Cal-27, HN-30, and HOK cell lines was detected by Western blot. A wound-healing assay was used to determine the effect of PTTG1 on the migration ability of the OSCC cells. The Transwell assay was used to examine the changes in cell-invasion ability. 5-ethynyl-2'-deoxyuridine (EdU) cell-proliferation assay was used to detect changes in cell-proliferation ability. Bioinformatics approach predicted the upstream miRNA of PTTG1. The targeting relationship between miR-362-3p and PTTG1 was examined by the dual luciferase assay, and quantitative real-time polymerase chain reaction (qRT-PCR) was used to determine the expression of miRNA in OSCC tissues.

Results: The ENCORI database showed that PTTG1 expression was up-regulated in OSCC tissues. Western blot confirmed that PTTG1 expression was up-regulated in Cal-27 and HN-30 cells than HOK cells. PTTG1 knockout can inhibit the migration, invasion, and proliferation of Cal-27 and HN-30 cells (P<0.05). Bioinformatics prediction websites predicted that the upstream miRNA of PTTG1 was miR-362-3p, and PTTG1 can bind to miR-362-3p. Results of qRT-PCR showed that miR-362-3p expression was downregulated in OSCC tissues compared with normal tissue (P<0.05). Transwell and EdU experiments confirmed that miR-362-3p knockdown can promote the invasion and proliferation of Cal-27 and HN-30 after PTTG1 knockdown.

Conclusions: miR-362-3p can inhibit the invasion and proliferation of Cal-27 and HN-30 cells by targeting PTTG1.

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