PURPOSE: The purpose of this study was to detect the expression pattern of SPZ1 in glioma samples and to clarify its biological functions in the malignant progression of glioma. Our results provide a novel molecular target for glioma. METHODS: SPZ1 levels in 40 pairs of glioma and non-tumoral ones were detected by quantitative real-time polymerase chain reaction (qRT-PCR). The differences in clinical indicators and prognosis between glioma patients expressing high and low levels of SPZ1 were compared. After knockdown of SPZ1 by transfection of sh-SPZ1, migratory and invasive abilities of A172 and U251 cells were examined by transwell migration and invasion assays. The interaction between SPZ1 and its target gene CXXC4 was finally explored by Western blot and dual-luciferase reporter assay. RESULTS: SPZ1 was upregulated in glioma tissues than non-tumoral ones, and the difference was statistically significant. Cell function experiments showed that knockdown of SPZ1 weakened the migratory and invasive abilities of A172 and U251 cells. CXXC4 was identified as the target gene binding to SPZ1. Knockdown of CXXC4 abolished the role of SPZ1 knockdown in inhibiting glioma progression. CONCLUSIONS: SPZ1 stimulates glioma's malignant progression via targeting CXXC4.
PURPOSE: The purpose of this study was to detect the expression pattern of SPZ1 in glioma samples and to clarify its biological functions in the malignant progression of glioma. Our results provide a novel molecular target for glioma. METHODS: SPZ1 levels in 40 pairs of glioma and non-tumoral ones were detected by quantitative real-time polymerase chain reaction (qRT-PCR). The differences in clinical indicators and prognosis between glioma patients expressing high and low levels of SPZ1 were compared. After knockdown of SPZ1 by transfection of sh-SPZ1, migratory and invasive abilities of A172 and U251 cells were examined by transwell migration and invasion assays. The interaction between SPZ1 and its target gene CXXC4 was finally explored by Western blot and dual-luciferase reporter assay. RESULTS: SPZ1 was upregulated in glioma tissues than non-tumoral ones, and the difference was statistically significant. Cell function experiments showed that knockdown of SPZ1 weakened the migratory and invasive abilities of A172 and U251 cells. CXXC4 was identified as the target gene binding to SPZ1. Knockdown of CXXC4 abolished the role of SPZ1 knockdown in inhibiting glioma progression. CONCLUSIONS: SPZ1 stimulates glioma's malignant progression via targeting CXXC4.