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. 2020 Aug 20;123(9):1445–1455. doi: 10.1038/s41416-020-01032-y

Fig. 5. E2F7−EZH2 axis triggers the AKT/mTOR pathway.

Fig. 5

a The mRNA levels of EZH2 and PTEN in E2F7-silenced cells were determined by qRT-PCR. b ChIP-qPCR analysis of EZH2 levels at PTEN promoter in LN229 and U251 cells expressing shCtrl or shE2F7. c ChIP-qPCR analysis of H3K27me3 levels at PTEN promoter in LN229 and U251 cells expressing shCtrl or shE2F7. d The expression of AKT, p-AKT, mTOR and p-mTOR in glioblastoma cells transduced with E2F7 shRNA clones or E2F7-overexpression vectors was examined by western blot. e The expression of E2F7, EZH2, PTEN, AKT, p-AKT, mTOR and p-mTOR in shE2F7 or shE2F7/EZH2 cells was determined by western blot. f The effect of EZH2 overexpression on the proliferation of E2F7-knockdown cells was shown by MTT assays. g Cells with shE2F7 or shE2F7/EZH2 were subjected to Transwell assays; the fold change of cell migration was presented. All data are shown as the mean ± SD, **p < 0.01, ***p < 0.001.