Down-regulation of β1,4GalT V at protein level contributes to arsenic trioxide-induced glioma cell apoptosis

Arsenic trioxide (As2O3) has considerable efficacy in treating solid tumors with induction of apoptosis with largely unknown mechanisms. Posttranslational processing of proteins by glycosylation could have multiple regulating roles in the process of apoptosis. Here, we found that the expression of β1,6-linked GlcNAc-bearing N-glycans on cell surface protein was gradually decreased after induction of apoptosis by As2O3-treatment. And, As2O3 significantly decreased the protein expression level of β1,4GalT V, which effectively galactosylates the β1,6-GlcNAc branch of N-glycans and functions as a positive regulator in glioma development. Furthermore, interfering with the expression of β1,4GalT V in human glioma cell markedly promoted As2O3-induced cell apoptosis and β1,4GalT V overexpression significantly reduced As2O3-induced glioma cell apoptosis. Taken together, our results suggested that down-regulation of β1,4GalT V expression plays an important role in As2O3-induced apoptosis, providing a new mechanism of As2O3-induced cell apoptosis and indicating that inhibitors of β1,4GalT V may enhance the therapeutic efficiency of As2O3 for malignant glioma.