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. 2022 Apr 19;13(4):373. doi: 10.1038/s41419-022-04827-4

Fig. 6. E2F1 was identified and confirmed as an upstream transcription factor of SLC7A11.

Fig. 6

A Prediction of potential upstream transcription factors of SLC7A11 in the oPOSSUM and GeneCards databases. B qRT-PCR showed that knockdown of E2F1 significantly suppressed the expression of SLC7A11. C Western blot analysis confirmed that E2F1 inhibition led to the downregulation of xCT expression in 293T cells. D, E The correlation between the expression of E2F1 and SLC7A11 in GSE17538 and GSE87211. F The potential binding sites of E2F1 to the SLC7A11 promoter region and binding site mutation strategy. G, H A luciferase assay was used to identify the binding sites of E2F1 to the SLC7A11 promoter region in 293T cells and HCT116 cells. I, J The expression of E2F1 was higher in CRC tissues than in normal samples from the TCGA-COAD cohort and TCGA-READ cohort. K Knockdown efficiency of E2F1 via lentiviral shRNA transfection was confirmed through western blot assay. L CCK-8 assay showed that E2F1 knockdown significantly inhibited the proliferation of HCT15 cells. M Transwell assays indicated that E2F1 inhibition effectively weakened the migration capability of HCT15 cells. N Sphere formation assays confirmed that E2F1 inhibition significantly suppressed the stemness of HCT15 cells. (O) Cell cycle assay showed E2F1 regulated cell cycle by inducing the G1/S transition. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001.