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. 2017 Dec 26;11(1):140–146. doi: 10.1016/j.tranon.2017.11.007

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© 2017 The Authors

This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

PMC Copyright notice

CHEK1-dependent RAD54L regulation is essential for proliferation and radioresistance of GBM cells.

(A) Top 30 genes correlated to CHEK1 mRNA expression in TCGA dataset. (B) Pearson or Spearman correlation analysis was performed to evaluate correlation between CHEK1 and RAD54L in TCGA dataset. (C) qRT-PCR analysis for CHEK1 mRNA expression in U87 cells treated with different dose of irradiation (P < .01, n = 3 with t test). (D) Western blotting analysis of U87 cells treated with different dose of irradiation. β-Actin served as a control. (E) qRT-PCR analysis indicated that RAD54L expression was elevated after U87 cells were exposed to radiotherapy, while these effects could be demolished by CHEK1 knockdown (P < .05, n = 3 with t test). (F) In vitro cell growth assay indicated that artificial knockdown of CHEK1 could enhance the radiosensitivity of U87 GBM cells (P < .05, n = 3 with t test). (G) Kaplan-Meier analysis was performed for the comparison of survival in U87-implanted mice treated with shNT or shCHEK1 and then compared with irradiation (P < .0001, with log-rank test).