Wang, Jubo; Quan, Yu; Lv, Jian; Gong, Shouping; Ren, Pengyu published the artcile< Inhibition of FAM83D displays antitumor effects in glioblastoma via down-regulation of the AKT /Wnt/β-catenin pathway>, Application In Synthesis of 112-63-0, the main research area is FAM83D antitumor glioblastoma; AKT; FAM83D; Wnt; glioblastoma.
Up-regulation of family with sequence similarity 83 member D (FAM83D) has been acknowledged as a vital contributor for the carcinogenesis of numerous cancers. The relevance of FAM83D in glioblastoma (GBM), however, is not well understood. This current work aimed to determine the possible roles and mechanisms of FAM83D in GBM. By analyzing The Cancer Genome Atlas (TCGA) data, we found dramatic increases in FAM83D expression in GBM tissue. We also observed elevated levels of FAM83D in the clin. specimens of GBM. In vitro data showed that silencing FAM83D resulted in remarkable antitumor effects via inhibiting the proliferation, invasion and epithelial-mesenchymal transition of GBM cells. Moreover, the knockdown of FAM83D improved sensitivity to the chemotherapy drug temozolomide. In-depth mechanism research revealed that the silencing of FAM83D strikingly decreased the phosphorylation levels of AKT and glycogen synthase kinase-3β, and prohibited activation of the Wnt/β-catenin pathway. The suppression of AKT abolished FAM83D-mediated activation of the Wnt/β-catenin pathway. The re-expression of β-catenin reversed FAM83D-silencing-induced antitumor effects in GBM cells. In addition, GBM cells with FAM83D silencing exhibited reduced tumorigenic potential in vivo. Overall, the data from this work show that the inhibition of FAM83D displays antitumor effects in GBM via down-regulation of the AKT/Wnt/β-catenin pathway and propose FAM83D as a new therapeutic target for GBM.
Environmental Toxicology published new progress about Antitumor agents. 112-63-0 belongs to class esters-buliding-blocks, and the molecular formula is C19H34O2, Application In Synthesis of 112-63-0.
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