FAM84B acts as a tumor promoter in human glioma via affecting the Akt/GSK-3β/β-catenin pathway

Family with sequence similarity 84, member B (FAM84B) has recently emerged as an oncoprotein in multiple types of cancer. However, whether FAM84B modulates the progression of glioma has not been determined. The goals of this work were to assess the possible relationship between FAM84B and glioma. Our data revealed high FAM84B level in glioma specimens and exhibited that the overexpression of FAM84B was correlated with a low survival rate in glioma patients. Cellular functional assays showed that silencing of FAM84B prohibited the proliferation and invasion, and induced the apoptosis of glioma cells. Further results determined that the knockdown of FAM84B remarkably decreased the levels of phosphorylated Akt and glycogen synthase kinase (GSK)-3 beta, and active beta-catenin. Inhibition of Akt abolished the FAM84B-mediated promotion effects on Wnt/beta-catenin pathway. The subcutaneous xenograft assay confirmed that the silencing of FAM84B significantly prohibited the tumorigenicity of glioma cells in vivo. Collectively, the findings from this work demonstrate that the downregulation of FAM84B exhibits a cancer-suppressive role in human glioma through the regulation of Akt/GSK-3 beta/beta-catenin pathway.

Automated summary

FAM84B has been identified as an oncoprotein in various cancers, and its overexpression in glioma is associated with low patient survival rates. Silencing FAM84B inhibits proliferation and invasion, induces apoptosis in glioma cells, and reduces phosphorylated Akt, GSK-3 beta, and active beta-catenin levels. Inhibition of Akt blocks the promotion effects of FAM84B on the Wnt/beta-catenin pathway. Additionally, in vivo experiments show that silencing FAM84B significantly suppresses the tumorigenicity of glioma cells.