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. 2024 Dec 18;46:27. doi: 10.1186/s41021-024-00321-9

Fig. 3.

Fig. 3

HSD17B6 inhibits LUAD cisplatin resistance via DNA damage. A Upset plot was used to visualize the intersection of the upstream potential transcription factors predicted by hTFtarget database and differentially downregulated genes; The x-axis represents the upstream potential transcription factor set of HSD17B6 predicted by hTFtarget, along with the set of differentially downregulated genes analyzed from the TCGA database. The intersection of these sets yields the potential upstream transcription factor set of HSD17B6. The y-axis represents the number of transcription factors and differentially expressed genes. B Pearson correlation diagram of GATA1 and HSD17B6; C The binding site map of transcription factor GATA1 and HSD17B6 in JASPAR database; The red box indicates multiple binding sites in the first 2000 bp region of the predicted HSD17B6 promoter, and “TTATTATCTTT 238–248” indicates the binding sites of GATA1 and HSD176 with the highest degree of matching with the predicted binding sites; D TCGA analysis of expression of GATA1 in LUAD tumor tissues and normal tissues; E, F qPCR and WB analysis of expression of GATA1 in human LUAD cell lines and human bronchial epithelial cells; G ChIP showed that GATA1 bound to the predicted site in the 2000 bp region upstream of the HSD17B6 promoter; H Dual-luciferase reporter assay further verified the interaction between GATA1 and HSD17B6 promoter. * means P < 0.05