TGFβ1-induced beta-site APP-cleaving enzyme 2 upregulation promotes tumorigenesis through the NF-κB signalling pathway in human gliomas.

摘要: Gliomas are the most common primary malignant tumours of central nervous system, and new molecular biomarkers urgently needed for diagnosis targeted therapy. Here, we report that increased beta-site APP-cleaving enzyme 2 (BACE2) expression is associated with increases in grade human glioma, incidence mesenchymal glioblastoma multiforme subtype likelihood poor prognoses patients. BACE2 knockdown suppressed cell invasion, migration tumour growth both vitro vivo, while overexpression promoted transition proliferation. Furthermore, TGFβ1 stimulated through Smad-dependent signalling, which modulated TNF-α-induced NF-κB activity PP1A/IKK pathway to promote tumorigenesis U87MG U251 cells. Our study indicated plays a significant role glioma development. Therefore, potential therapeutic target gliomas due its function ability be regulated.