This study was to determine the Semaphorin3B(SEMA3B) role in glioma cells responding to irradiation. Two glioma cell lines,which were used here was wild-type p53(U-87MG),and the other was harboring mutated p53 (U-251).The SEMA3B mRNA could be detected in the two cell lines.The expression level of SEMA3B mRNA was higher in U-87MG cells than in U-251 cells,and increased with time in U-87MG cells after irradiation.Knockdown of SEMA3B expression by shRNA decreased the radiosensitivity of U-87MG cells,this may be associated with the increased G2 accumulation after irradiation.In addition,G2 accumulation after irradiation was enhanced in SEMA3B low-expressing U-87MG cells.These results showed that the SEMA3B was implicated in glioma cells responding to irradiation.
LIU HaiyanXU YuanvuanCHEN YunJIANG XinYU JiahuaYANG LeiGU ChengLIU Fenju
Radiation therapy plays a critical role in the treatment of neurogliocytoma and it is known that doublecortin (DCX)-transfected U87 cells can inhibit tumor cell growth. Microarray analysis to screen for differentially expressed genes in DCX-transfected U87 cells before and after radiation uncovered DCX-related genes, the functions of DCX, and downstream genes in radiation therapy of neurogliocytoma. Stably transfected U87 cells were constructed (DCX-U87) and the differentially expressed genes were screened by microarray analysis to compare U87 cells with DCX-U87 cells in both non-irradiated and irradiated conditions. Cells were irradiated using 60Co γ-ray at a dose rate of 1.0 Gy/min. Mean values were subject to paired comparison analysis and genes with a p-value of less than 0.05 were analyzed. Differentially expressed genes can correlate with radiation sensitivity and DCX transfection. DCX and SPN proteins in DCX-U87 cells were detected by two groups of 0 and 10 Gy, but not the U87 cells, and their expression levels were higher in the 10 Gy group than in the 0 Gy group. The differential gene expression in DCX-U87 cells before and after radiation is helpful for future investigations into the mechanisms of radiation therapy in neurogliocytoma cells.
