中文摘要：

<正>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.

英文摘要：

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.