信号转导和转录激活因子1通过激活黏着斑激酶（FAK）信号通路的磷酸化来促进胶质瘤的迁移和增殖，并阻止其凋亡。
SIPA1 boosts migration and proliferation, and blocks apoptosis of glioma by activating the phosphorylation of the FAK signaling pathway.
作者信息
Du Yuan, Li Shenglan, Zhou Tong, Zhao Jing, Liu Jiguang
机构信息
Jiamusi University, School of Basic Medicine Science, Jiamusi, China.
Capital Medical University, Beijing Tiantan Hospital, Department of Neuro-oncology, Cancer center, Beijing, China.
出版信息
J Med Biochem. 2022 Feb 2;41(1):108-114. doi: 10.5937/jomb0-32903.
BACKGROUND
We aimed to analyze the regulatory effects of SIPA1 (signal-induced proliferation-associated protein 1) on glioma progression and the dominant signaling pathway.
METHODS
Differential 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.
RESULTS
SIPA1 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.
CONCLUSIONS
SIPA1 is upregulated in glioma that boosts migratory and proliferative potentials of glioma cells by activating the phosphorylation of the FAK signaling pathway.
背景
我们旨在分析信号诱导增殖相关蛋白1（SIPA1）对胶质瘤进展的调控作用以及主要信号通路。
方法
测定胶质瘤组织和正常组织及细胞中SIPA1的差异水平。检测过表达或敲低SIPA1的A172细胞的迁移、增殖、凋亡及细胞周期进程变化。最后，检测SIPA1及FAK抑制剂PF562271干预的A172细胞中磷酸化FAKs的蛋白水平。
结果
胶质瘤病例中SIPA1上调。敲低SIPA1可降低胶质瘤细胞的迁移和增殖率，增加凋亡细胞率，并降低S期细胞比例。敲低SIPA1还下调细胞周期蛋白。此外，SIPA1上调A172细胞中磷酸化FAKs，从而增强胶质瘤的恶性表型。
结论
胶质瘤中SIPA1上调，通过激活FAK信号通路的磷酸化增强胶质瘤细胞的迁移和增殖潜能。
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