Abstract
INTRODUCTION: Glioma is the most common primary intracranial tumour that is highly resistant to conventional therapeutic approaches including surgical resection, radiation therapy, and chemotherapy. As a promising alternative treatment, gene therapy has achieved variable degrees in both pre-clinical models and clinical trials. MATERIAL AND METHODS: In our present research, the role of calcium binding and coiled-coil domain 2 (CALCOCO2) in the pathogenesis and progression of glioma was investigated in human glioma U87 and U251 cell lines. In both cell lines, CALCOCO2 is highly expressed. Targeted by lentivirus vectors, the CALCOCO2 gene was successfully silenced in U87 and U251 cell lines. Both cell counting and MTT assay showed the inhibition of cell growth and cell proliferation in CALCOCO2-silenced glioma cell lines. RESULTS: Flow cytometry (FCM) and caspase3/7 measurements indicated that the silencing of CALCOCO2 gene could also promote cell apoptosis in both cell lines. The underlying mechanism was further explored by gene microarray and western blotting. The CALCOCO2 gene is strongly related to cancer by affecting the expression of hundreds of genes. Among which, the silencing of CALCOCO2 significantly upregulated the pro-apoptosis genes FAS and CASP1 and downregulated the autophagy-related gene BECN1. These data suggest that by regulating FAS, CASP1, and BECN1, the silencing of CALCOCO2 suppresses the growth and proliferation of U87 and U251 glioma cell lines. CONCLUSIONS: The CALCOCO2 could be a potential target for glioma genetic therapy.