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SYT7 的下调通过促进细胞凋亡抑制胶质母细胞瘤的生长。

Downregulation of SYT7 inhibits glioblastoma growth by promoting cellular apoptosis.

机构信息

Department of Neurosurgery, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, P.R. China.

Department of Neurosurgery, The Second Hospital of Nanchang, Nanchang, Jiangxi 330003, P.R. China.

出版信息

Mol Med Rep. 2017 Dec;16(6):9017-9022. doi: 10.3892/mmr.2017.7723. Epub 2017 Oct 4.

DOI:10.3892/mmr.2017.7723
PMID:28990113
Abstract

Synaptotagmin‑7 (SYT7) is a member of the synaptotagmin gene family, and encodes a protein that mediates the calcium‑dependent regulation of membrane trafficking during synaptic transmission. A previous study demonstrated that the expression of SYT7 is associated with prostate cancer and serves an important role in development of prostate cancer. However, the roles of SYT7 in the progression of glioma remain unknown. In the present study, reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) analysis demonstrated that SYT7 was expressed in three human glioma cell lines. Western blotting and RT‑qPCR analysis demonstrated the knockdown efficiency of SYT7 shRNA in 293T cells and U87MG cells. Celigo Image Cytometer Analysis, a caspase‑3/7 assay, flow cytometry and an MTT assay demonstrated that the proliferation of U87MG cells was inhibited as SYT7 was downregulated by a lentiviral vector expressing SYT7 shRNA, via the promotion of cellular apoptosis. The results of the present study demonstrated that the downregulation of SYT7 inhibited glioblastoma growth by promoting cellular apoptosis, and that SYT7 may therefore be a potential target for glioma intervention.

摘要

突触结合蛋白 7(SYT7)是突触结合蛋白基因家族的成员,编码一种蛋白,该蛋白在突触传递过程中通过钙依赖性调节膜转运而起作用。先前的研究表明,SYT7 的表达与前列腺癌相关,并在前列腺癌的发展中发挥重要作用。然而,SYT7 在神经胶质瘤进展中的作用尚不清楚。在本研究中,逆转录-定量聚合酶链反应(RT-qPCR)分析表明 SYT7 在三种人神经胶质瘤细胞系中表达。Western blot 和 RT-qPCR 分析表明 SYT7 shRNA 在 293T 细胞和 U87MG 细胞中的敲低效率。Celigo 图像细胞仪分析、半胱天冬酶-3/7 测定、流式细胞术和 MTT 分析表明,通过表达 SYT7 shRNA 的慢病毒载体下调 SYT7 可促进细胞凋亡,从而抑制 U87MG 细胞的增殖。本研究的结果表明,下调 SYT7 通过促进细胞凋亡抑制胶质母细胞瘤的生长,因此 SYT7 可能是神经胶质瘤干预的潜在靶点。

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