Myristoylated alanine rich protein kinase C substrate is a potential cancer prognostic factor that regulates cell migration and invasion in glioblastoma

被引:2
作者
Xiang, Wei [1 ]
Peng, Tao [1 ]
Ming, Yang [1 ]
Li, Shenjie [1 ]
Wang, Ke [1 ]
Wang, Haorun [1 ]
Chen, Ligang [1 ]
Zhou, Jie [1 ]
机构
[1] Southwest Med Univ, Dept Neurosurg, Affiliated Hosp, 25 Taiping St, Luzhou 646000, Sichuan, Peoples R China
关键词
epithelial-mesenchymal transition; glioblastoma; MARCKS; phosphoinositide 3-kinase/protein kinase B; TRANSCRIPTION FACTOR SNAIL; MESENCHYMAL TRANSITION; MOLECULAR-MECHANISMS; GENE-EXPRESSION; MARCKS; GROWTH; RESISTANCE; CARCINOMA; PROLIFERATION; CONTRIBUTE;
D O I
10.3892/or.2019.7009
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Myristoylated alanine-rich C-kinase substrate (MARCKS) serves an important role in various pathological processes in several malignancies. However, little is known about the specific role and molecular mechanism of MARCKS in glioblastoma (GBM). In the present study, it was found that the expression of MARCKS was significantly upregulated in GBM, and was associated with a poor clinical outcome in patients with GBM. Knockdown of MARCKS suppressed the migration and invasion of GBM cells in vitro. Western blotting showed that the knockdown of MARCKS reduced the expression of phosphorylated phosphoinositide 3-kinase and protein kinase B, as well as zinc finger protein SNAI1 expression, thereby modulating the expression of its downstream epithelial-mesenchymal transition (EMT)-associated factors, including E-cadherin, vimentin, N-cadherin and beta-catenin in GBM cells. These results indicate that MARCKS functioned in the migration and invasion of GBM, and therefore may provide a potential therapeutic target in GBM therapy.
引用
收藏
页码:2464 / 2470
页数:7
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