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TIPE2 Inhibits Hypoxia-Induced Wnt/beta-Catenin Pathway Activation and EMT in Glioma Cells

机译:TIPE2抑制低氧诱导的胶质瘤细胞Wnt /β-Catenin途径激活和EMT。

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摘要

Hypoxia-induced epithelial-to-mesenchymal transition (EMT) could facilitate tumor progression. TIPE2, the tumor necrosis factor-alpha (TNF-alpha)-induced protein 8-like 2 (also known as TNFAIP8L2), is a member of the TNF-alpha-induced protein 8 (TNFAIP8, IWE) family and has been involved in the development and progression of several tumors. However, the effects of TIPE2 on the EMT process in glioma cells and the underlying mechanisms of these effects have not been previously reported. In our study, we assessed the roles of TIPE2 in the EMT process in glioma cells in response to hypoxia. Our results indicated that TIPE2 expression was significantly decreased in human glioma cell lines. TIPE2 overexpression significantly inhibited hypoxia-induced migration and invasion, as well as suppressed the EMT process in glioma cells. Furthermore, TIPE2 overexpression prevented hypoxia-induced expression of beta-catenin, cyclin D1, and c-myc in human glioma cells. In summary, these data suggest that TIPE2 overexpression inhibited hypoxia-induced Wnt/beta-catenin pathway activation and EMT in glioma cells.
机译:缺氧诱导的上皮-间质转化(EMT)可能促进肿瘤进展。 TIPE2是肿瘤坏死因子-α(TNF-α)诱导的蛋白8-like 2(也称为TNFAIP8L2),是TNF-α诱导的蛋白8(TNFAIP8,IWE)家族的成员,并且已经参与几种肿瘤的发生和发展。但是,TIPE2对神经胶质瘤细胞EMT过程的影响以及这些作用的潜在机制尚未见报道。在我们的研究中,我们评估了TIPE2在神经胶质瘤细胞对缺氧反应中EMT过程中的作用。我们的结果表明,在人神经胶质瘤细胞系中TIPE2表达明显降低。 TIPE2的过表达显着抑制了缺氧诱导的迁移和侵袭,并抑制了胶质瘤细胞的EMT过程。此外,TIPE2的过表达可防止缺氧诱导人胶质瘤细胞中β-catenin,cyclin D1和c-myc的表达。总之,这些数据表明TIPE2过表达抑制了神经胶质瘤细胞缺氧诱导的Wnt /β-catenin途径激活和EMT。

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