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Fig. 3 | Journal of Experimental & Clinical Cancer Research

Fig. 3

From: Epigenetic regulation of ferroptosis via ETS1/miR-23a-3p/ACSL4 axis mediates sorafenib resistance in human hepatocellular carcinoma

Fig. 3

ETS1 directly stimulates miR-23a-3p transcription upon sorafenib treatment. A The expression of miR-23a-3p and B pri-miR-23a in MHCC97L and PLC/PRF/5 cells treated with sorafenib for 24 h. The doses of sorafenib were corresponding to 0, IC10, IC15, and IC20 values of sorafenib. C Venn diagram showing the intersections of data from proteomics analysis, ChIP-X, TransmiR and Circuit. Three TFs: ETS1, NFIC, and SP1 were the common TFs. D Gene ranking of potential TFs of proteomics data according to their log2FC. ETS1 was the highest upregulated TF. E The expression of miR-23a-3p in MHCC97L and F PLC/PRF/5 by qRT-PCR and the expression of ETS1 by immunoblotting. G Luciferase activity of pGL-23AP639 in HEK293. One-way ANOVA, p < 0.005***, p < 0.0001****. H The binding motif of ETS-1 on miR-23a promoter and the fold enrichment of fragments of miR-23a promoter was higher in sorafenib treated MHCC97L after the pulldown by ETS-1 Ab. The IgG Ab group was set as the negative control. Unpair t-test, p < 0.0001****

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