SIPA1 boosts migration and proliferation, and blocks apoptosis of glioma by activating the phosphorylation of the FAK signaling pathway.

Yuan Du,Jiguang Liu,Jing Zhao,Shenglan Li,Tong Zhou

doi:10.5937/jomb0-32903

Abstract

BackgroundWe aimed to analyze the regulatory effects of SIPA1 (signal-induced proliferation-associated protein 1) on glioma progression and the dominant signaling pathway.MethodsDifferential level of SIPA1 in glioma and normal tissues and cells was determined. Migratory, proliferative, apoptotic and cell cycle progression changes in A172 cells with overexpression or knockdown of SIPA1 were examined. Finally, protein levels of phosphorylated FAKs in A172 cells intervened by SIPA1, and the FAK inhibitor PF562271 were detected.ResultsSIPA1 was upregulated in glioma cases. Knock-down of SIPA1 reduced migratory and proliferative rates of glioma cells, increased apoptotic cell rate, and declined cell ratio in the S phase. The knockdown of SIPA1 also downregulated cell cycle proteins. In addition, SIPA1 upregulated phosphorylated FAKs in A172 cells and thus boosted malignant phenotypes of glioma.ConclusionsSIPA1 is upregulated in glioma that boosts migratory and proliferative potentials of glioma cells by activating the phosphorylation of the FAK signaling pathway.

Highlights

Gliomas are the leading malignant tumors of the central nervous system that originate from glial cells of the neuroectoderm
SIPA1 is upregulated in glioma that boosts migratory and proliferative potentials of glioma cells by activating the phosphorylation of the FAK signaling pathway
This study aims to explore the regulatory effects of SIPA1 on glioma and the dominant signaling pathway

Summary

Introduction

Gliomas are the leading malignant tumors of the central nervous system that originate from glial cells of the neuroectoderm. They represent 80% of primary intracranial malignancies [1]. The average survival time of glioma is only 12–14 months [2]. Surgery combined radiotherapy, chemotherapy and biotherapy is preferred to glioma patients, they can only prolong the survival for months. The prognosis of glioma is extremely poor [3]. Clarification of the pathogenesis of glioma and the involvement of differentially expressed genes in glioma contributes to the improvement of clinical outcomes [4]

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