Abstract:

Objective To investigate the differences and causes of glioblastoma cell linesof different geno⁃ typesin radiation resistance. Methods Three GBM cell lines with different genotypes （U87MG，U251MG， U118MG）were selected. P53 and PTEN gene mutations were detected by exon sequencing technology，and MGMT expression was detected by Western blotting. After irradiation withdifferent doses（2 Gy，5 Gy，10 Gy），flow cytometry was used to detect the levels of apoptosis，and plate clone formation to detect cell proliferations，so that the radia⁃ tion resistance was analyzed. Western blot was used to detect the activation of DNA damage marker protein （γH2AX），NF⁃κB effector molecule（RELA/p65）and EGFR within 48 hours after radiation，followed byanalyz⁃ ing the correlation between DNA damage and the activation of NF ⁃ κB and EGFR signaling pathways. Results U87MG，U251MG，and U118MG all hadmutation sites of P53 and PTEN. Among them，U87MG and U251MG low⁃expressed MGMT，and U118MG high⁃expressed MGMT. After 48 hradiation with the doses of 2 Gy，5 Gy，and 10 Gy，there was a change inthe apoptosis rate：U87MG > U118MG > U251MG，and at the survival score： U251MG > U118MG > U87MG across the four doses. There were differences in the activation time and dose of γH2AX，RELA/p65 and EGFR in the three cell lines after irradiation. Conclusion Radiation resistance：U251MG has the highest radiation resistance，followed by U118MG and U87MG in sequence，which suggests that the radia⁃ tion resistance of GBM cell line is related to its genotypes. There are differences in the activation of the NF ⁃ κB pathway and the EGFR pathway after irradiation to the three cell lines，which ultimately leads to differences in their radiation resistance. 

Key words:

glioblastoma, ionizing radiation, radiation resistance