The treatment effects and the underlying mechanism of B cell translocation gene 1 on the oncogenesis of brain glioma.

Abstract

Glioma is characterized by cell over-proliferation, aggressive phenotype, and angiogenesis. B cell translocation gene 1 (BTG1) works as a tumor suppressor in various cancer types. We aimed to study the functions of BTG1 in glioma development. We tested the BTG1 expressions in various glioma cell lines. T98G and U87 cells were transfected with siBTG1 and BTG1 expression vector, respectively, then assessing cell viability, cell migration, and invasion abilities. Flow cytometry was performed to analyze apoptosis and cell cycle distribution. The status of angiogenesis was assessed by In vitro angiogenesis assay. Quantitative polymerase chain reaction and Western blot analysis were used for expression analyses. The inhibitor FH535 (20 μM) and agonist LiCl (20 mM) of the Wnt/β-catenin pathway were introduced to treat transfected cells. BTG1 was low-expressed in glioma cell lines. In T98G cell transfected with siBTG1, cell proliferation, migration, invasion, and angiogenesis abilities were notably increased, BTG1 silencing promoted the cell survival and cell cycle progression from G0/G1 to the S phase. In BTG overexpressed U87 cell, cell proliferation, migration, invasion, and angiogenesis abilities were significantly inhibited. In addition, cell apoptosis significantly increased and the number of G0/G1 phase cells was also significantly increased. We also found that the activation of Wnt/β-catenin was significantly inhibited in BTG1 group. LiCl and FH535 treatments could partially reverse the effects of BTG1 on glioma cell viabilities. Our data suggested that BTG1 functions as a tumor suppressor in glioma, and the anticancer ability of BTG1 involves the repression of the Wnt/β-catenin pathway.