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miR-650 通过靶向 FAM83F 抑制神经胶质瘤的进展。

MiR-650 inhibits the progression of glioma by targeting FAM83F.

机构信息

Department of Neurosurgery, Central People's Hospital of Zhanjiang, Zhanjiang, China.

出版信息

Eur Rev Med Pharmacol Sci. 2018 Dec;22(23):8391-8398. doi: 10.26355/eurrev_201812_16537.

Abstract

OBJECTIVE

The aim of this study was to explore whether miR-650 could inhibit the proliferation of glioma by regulating FAM83F and to investigate the specific role of miR-650 in glioma occurrence.

PATIENTS AND METHODS

The expression of FAM83F in tumor or para-cancerous tissues of 24 glioma patients was detected by quantitative real-time polymerase chain reaction (qRT-PCR). Meanwhile, FAM83F expression in 6 glioma cell lines (LN229, U87, U251, LN308, SNB19 and H4) was also detected. Subsequently, the proliferation of glioma cells transfected with miR-650 mimics was evaluated by cell counting kit-8 (CCK-8) and EDU (5-ethynyl-2'-deoxyuridine) assay, respectively. In addition, Luciferase reporter gene assay and rescue experiment were applied to verify the relationship between miR-650 and FAM83F.

RESULTS

MiR-650 expression in glioma tissues was significantly decreased, while the expression of FAM83F was remarkably upregulated. This indicated that the level of miR-650 was negatively correlated with that of FAM83F. Similar results were obtained in glioma cells. We then transfected miR-650 mimics into LN229 and U251 cells, and found that the expression of miR-650 was significantly upregulated. Meanwhile, the viability of cells significantly decreased. In addition, the interaction between miR-650 and FAM83F was verified by Luciferase reporter gene assay. Rescue experiments showed that miR-650 could inhibit cell proliferation by targeting FAM83F.

CONCLUSIONS

MiR-650 was lowly expressed in glioma tissues, which could promote cell proliferation through up-regulating the expression of FAM83F.

摘要

目的

本研究旨在探讨 miR-650 是否可以通过调控 FAM83F 来抑制神经胶质瘤的增殖,并研究 miR-650 在神经胶质瘤发生中的具体作用。

患者与方法

通过实时定量聚合酶链反应(qRT-PCR)检测 24 例神经胶质瘤患者肿瘤或癌旁组织中 FAM83F 的表达情况。同时,检测 6 种神经胶质瘤细胞系(LN229、U87、U251、LN308、SNB19 和 H4)中 FAM83F 的表达情况。然后,通过细胞计数试剂盒-8(CCK-8)和 EDU(5-乙炔基-2'-脱氧尿苷)检测转染 miR-650 模拟物的神经胶质瘤细胞的增殖情况。此外,应用荧光素酶报告基因检测和挽救实验来验证 miR-650 和 FAM83F 之间的关系。

结果

神经胶质瘤组织中 miR-650 的表达明显降低,而 FAM83F 的表达明显上调。这表明 miR-650 的水平与 FAM83F 的水平呈负相关。在神经胶质瘤细胞中也得到了类似的结果。随后,我们将 miR-650 模拟物转染到 LN229 和 U251 细胞中,发现 miR-650 的表达明显上调,同时细胞活力显著下降。此外,荧光素酶报告基因检测验证了 miR-650 和 FAM83F 之间的相互作用。挽救实验表明,miR-650 可以通过靶向 FAM83F 抑制细胞增殖。

结论

miR-650 在神经胶质瘤组织中低表达,可通过上调 FAM83F 的表达促进细胞增殖。

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