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首页> 外文期刊>Journal of cellular physiology. >MiR-34a inhibits the proliferation, migration, and invasion of oral squamous cell carcinoma by directly targeting SATB2
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MiR-34a inhibits the proliferation, migration, and invasion of oral squamous cell carcinoma by directly targeting SATB2

机译：MiR-34a抑制扩散、迁移和口腔鳞状细胞癌的侵犯直接针对SATB2

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摘要

In various kinds of carcinomas, the special AT-rich sequence-binding protein 2 (SATB2) with its atypical expression promotes the metastasis and progression of the tumor, though in the oral squamous cell carcinoma (OSCC) its inherent mechanism and the status of SATB2 remain unclear. The role played by the SATB2 expression in the OSCC cell lines and tissue samples in the target of miR-34a downstream is the intended endeavor of this study. In te OSCCs the miR-34a expression was determined by quantitative real-time polymerase chain reaction (q-PCR), while the SATB2 expression in the cell lines and tissue samples in OSCC was analyzed with the q-PCR and the western blot. Studies in both in vitro and in vivo of the effects of miR-34a on the initiation of OSCC were conducted. As a direct target of the miR-34a the SATB2 was verified with the luciferase reporter assay. In cases where the miR-34a levels were low, the SATB2 in OSCCs seemed to be overexpressed. Besides, both in the in vitro and in vivo a suppression of migration, invasion, and cell growth was caused by miR-34a by down regulating the SATB2 expression. The SATB2 being a direct target of miR-34a was confirmed by the cotransfection of miR-34a mimics specifically the decrease in the expression of luciferase of SATB2-3'UTR-wt reporter. As a whole, our study confirmed the inhibition of miR-34a in the invasion, proliferation, and migration of the OSCCs, playing a potential tumor suppressor role with SATB2 as its downstream target.
机译：在各种各样的癌,特别at富集sequence-binding蛋白2 (SATB2)其典型表现促进转移和肿瘤的进展,尽管口服鳞状细胞癌(OSCC)其固有的机制和SATB2的地位尚不清楚。SATB2表达式中所扮演的角色OSCC细胞系和组织样本的目标miR-34a下游的目标努力本研究。是由定量实时聚合酶链反应(q-PCR),SATB2表达细胞系和组织样品在OSCC q-PCR和分析免疫印迹。体内的影响miR-34a起始OSCC的进行。miR-34a SATB2验证的荧光素酶记者分析。miR-34a水平低,OSCCs SATB2似乎是过表达。在体外和体内迁移的抑制,入侵,细胞生长是由miR-34a引起的通过调节SATB2表达式。SATB2 miR-34a的直接目标确认的cotransfection miR-34a模仿具体的表达减少荧光素酶的SATB2-3'UTR-wt记者。整体而言,我们的研究证实了抑制miR-34a入侵,扩散OSCCs迁移,发挥潜在的肿瘤抑制作用与SATB2作为其下游目标。

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