Fig. 3: ZFP82 enhances esophageal carcinoma chemo-sensitivity through interacting with HDAC3. | Cell Death & Disease

Fig. 3: ZFP82 enhances esophageal carcinoma chemo-sensitivity through interacting with HDAC3.

From: Zinc Finger Protein 82 regulates p53 protein stability through histone deacetylase and enhances neo-adjuvant chemotherapy in esophageal cancer

Fig. 3

A RNA-seq shows in ZFP82 over-expressing cell lines compared to vector cells, significantly differentially expressed genes including molecules related to the p53 signaling pathway. B The volcano plot of differentially expressed genes includes HDAC3, which is significantly downregulated by ZFP82. C The regulatory effect of ZFP82 on HDAC3 and p53 signaling pathway genes was verified by qPCR. (**, p < 0.01). D Luciferase reporter assay results confirm that ZFP82 directly regulates the transcription of HDAC3. E Possible ZFP82-HDAC3 binding sites predicts by JASPAR database. F The binding of ZFP82 to the HDAC3 promoter was confirmed in both cell lines by ChIP-qPCR. G Identification of interaction between ZFP82 and HDAC3 by immunocoprecipitation assay. H ZFP82 inhibits HDAC3 activity by HDAC3 activity assay, (**, p < 0.01). I Ectopic expression of ZFP82 induced partial cytoplasmic translocation of HDAC3 in KYSE950/R cells as observed by immunofluorescence. J On ZFP82 over-expression KYSE950/R model, in the presence of chemo-reagent 5-FU (10 μg/mL), ZFP82 induced HDAC3 cleavage, caspases 3 cleavage, Fas, FasL expression in a time depended manner by Western blot (HDAC3-N antibody recognizes endogenous levels of total HDAC3 protein, HDAC3-C antibody raised against the C-terminus of HDAC3). K GSEA enrichment analysis shows that ZFP82 is related to the p53 signaling pathway.

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