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通过泛素连接酶Nedd4-1修饰Rap2a活性来调控胶质瘤的迁移和侵袭

Regulation of glioma migration and invasion via modification of Rap2a activity by the ubiquitin ligase Nedd4-1.

作者信息

Wang Lei, Zhu Bingxin, Wang Shiquan, Wu Yuxuan, Zhan Wenjian, Xie Shao, Shi Hengliang, Yu Rutong

机构信息

Insitute of Nervous System Diseases, Xuzhou Medical University, Xuzhou, Jiangsu, P.R. China.

出版信息

Oncol Rep. 2017 May;37(5):2565-2574. doi: 10.3892/or.2017.5572. Epub 2017 Apr 11.

Abstract

Νeuronal precursor cell expressed and developmentally downregulated protein (Nedd4-1) is an E3 ubiquitin ligase with critical roles in the pathogenesis of cancer. Herein, we demonstrated that Nedd4-1 protein was upregulated in glioma tissues vs. that in non-cancerous tissues by western blotting and immunohistochemistry. Scratch migration and Transwell chamber assays indicated that downregulation of Nedd4-1 significantly reduced the migration and invasion of the glioma cell lines U251 and U87. Conversely, overexpression of Nedd4-1 obviously enhanced the migratory and invasive capacities in both cell lines. To investigate the role of Nedd4-1 and the intracellular pathways involved, we performed pull-down and co-immunoprecipitation assays, and recognized that Nedd4-1, TNIK and Rap2a formed a complex. Moreover, Nedd4-1 selectively ubiquitinated its specific substrates, the wild-type Rap2a (WT-Rap2a) and dominant-active Rap2a (DA-Rap2a) rather than the dominant-negative Rap2a (DN-Rap2a) in the U251 cells. Subsequently, we demonstrated that Rap2a was robustly ubiquitinated by Nedd4-1 along with the K63-linked, but not the K48-linked ubiquitin chain, which significantly inhibited GTP-Rap2a activity by GST-RalGDS pull-down assay. To further verify whether the ubiquitination of Rap2a by Nedd4-1 regulated the migration and invasion of glioma cells, Nedd4-1, HA-tagged ubiquitin and its mutants as well as WT-Rap2a were co-transfected in the U251 and U87 cell lines. The results confirmed that Nedd4-1 inhibited GTP-Rap2a activity, and promoted the migration and invasion of glioma cells. In brief, our findings demonstrated the important role of Nedd4-1 in regulating the migration and invasion of glioma cells via the Nedd4-1/Rap2a pathway, which may qualify Nedd4-1 as a viable therapeutic target for glioma.

摘要

神经元前体细胞表达且发育下调蛋白(Nedd4-1)是一种E3泛素连接酶,在癌症发病机制中起关键作用。在此,我们通过蛋白质印迹法和免疫组织化学证明,与非癌组织相比,神经胶质瘤组织中Nedd4-1蛋白上调。划痕迁移和Transwell小室试验表明,Nedd4-1的下调显著降低了胶质瘤细胞系U251和U87的迁移和侵袭能力。相反,Nedd4-1的过表达明显增强了两种细胞系的迁移和侵袭能力。为了研究Nedd4-1的作用以及涉及的细胞内途径,我们进行了下拉和免疫共沉淀试验,并发现Nedd4-1、TNIK和Rap2a形成了一个复合物。此外,在U251细胞中,Nedd4-1选择性地泛素化其特定底物野生型Rap2a(WT-Rap2a)和显性激活型Rap2a(DA-Rap2a),而不是显性负性Rap2a(DN-Rap2a)。随后,我们证明Rap2a被Nedd4-1强烈泛素化,且伴随着K63连接而非K48连接的泛素链,通过GST-RalGDS下拉试验,这显著抑制了GTP-Rap2a活性。为了进一步验证Nedd4-1对Rap2a的泛素化是否调节胶质瘤细胞的迁移和侵袭,将Nedd4-1、HA标记的泛素及其突变体以及WT-Rap2a共转染到U251和U87细胞系中。结果证实,Nedd4-1抑制GTP-Rap2a活性,并促进胶质瘤细胞的迁移和侵袭。简而言之,我们的研究结果证明了Nedd4-1在通过Nedd4-1/Rap2a途径调节胶质瘤细胞迁移和侵袭中的重要作用,这可能使Nedd4-1成为胶质瘤的一个可行治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4611/5428538/4ca336ebae6d/OR-37-05-2565-g00.jpg

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