SPOCK1 promotes the proliferation, migration and invasion of glioma cells through PI3K/AKT and Wnt/β-catenin signaling pathways

被引：56

作者：

Yang, Jinghui ^{[1
]}

Yang, Qiwei ^{[2
]}

Yu, Jing ^{[3
]}

Li, Ximeng ^{[4
]}

Yu, Shan ^{[3
]}

Zhang, Xuewen ^{[1
]}

机构：

[1] Jilin Univ, China Japan Union Hosp, Dept Hepatopancreatobiliary Surg, 126 Xiantai St, Changchun 130033, Jilin, Peoples R China

[2] Jilin Univ, Hosp 2, Cent Lab, Changchun 130041, Jilin, Peoples R China

[3] Jilin Univ, China Japan Union Hosp, Dept Nephrol, 126 Xiantai St, Changchun 130033, Jilin, Peoples R China

[4] Jilin Univ, Coll Basic Med Sci, Cent Lab, Changchun 130012, Jilin, Peoples R China

来源：

ONCOLOGY REPORTS | 2016年 / 35卷 / 06期

关键词：

SPOCK1; glioma; proliferation; migration; invasion; PI3K/AKT; Wnt/beta-catenin; EPITHELIAL-MESENCHYMAL TRANSITION; CENTRAL-NERVOUS-SYSTEM; MALIGNANT GLIOMAS; IV COLLAGENASE; C-MYC; ELEVATED LEVELS; UP-REGULATION; BETA-CATENIN; CANCER-CELLS; LUNG-CANCER;

D O I：

10.3892/or.2016.4757

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Sparc/osteonectin, cwcv and kazal-like domains proteoglycan (testican) 1 (SPOCK1) has been reported to promote the growth and progression of various tumors. In this study, we focus on assessing the effect of SPOCK1 on proliferation, migration and invasion in glioma cells and elucidating its related mechanisms. The results of our present study demonstrated that overexpression of SPOCK1 promoted the proliferation and inhibited apoptosis in glioma cells. Additionally, overexpression of SPOCK1 promoted the migration and invasion potential of glioma cells. Moreover, we demonstrated that PI3K/AKT and Wnt/beta-catenin signaling pathways were activated by SPOCK1 overexpression. SPOCK1 silencing has precisely the opposite effect. In conclusion, our study suggests that SPOCK1 promotes proliferation, migration and invasion in glioma cells by activating PI3K/AKT and Wnt/P-catenin pathways, which provides a potential theoretical basis for clinical treatment of glioma.

引用

页码：3566 / 3576

页数：11

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