Fig. 6: Intracellular NOTCH4 (NICD4) transactivates HES1 by competitive binding with its gene promoter over p-STAT3. | Nature Communications

Fig. 6: Intracellular NOTCH4 (NICD4) transactivates HES1 by competitive binding with its gene promoter over p-STAT3.

From: NOTCH4ΔL12_16 sensitizes lung adenocarcinomas to EGFR-TKIs through transcriptional down-regulation of HES1

Fig. 6

a ChIP analysis of NOTCH4 binding to the HES1 promoter in 293 T cells and luciferase analysis of NOTCH4 to HES1. (n = 3 biologically independent experiments). b The predicted binding sites of STAT3 and NICD4 to HES1 promoter. c ChIP analysis of NOTCH4 and p-STAT3 binding to the HES1 promoter in 293 T cells. (n = 3 biologically independent experiments). d Luciferase analysis of NOTCH4 and STAT3 to HES1 in 293 T cells (n = 3 biologically independent experiments). e Western blot analysis in PC-9GR/PC-9OR. f and g ChIP analysis of NOTCH4 and p-STAT3 binding to the HES1 promoter in PC-9GR/PC-9OR cells treated with siNOTCH4 or siSTAT3. (n = 3 biologically independent experiments). h and j The tumor growth curve of CDX models with siNOTCH4, siSTAT3 or their combination treatments. (n = 5 CDXs). (i and k) The tumor weight of CDX models with siNOTCH4, siSTAT3 or their combination treatment. (n = 5 CDXs). l and n The tumor growth curve of PDX models of PC-9GR/PC-9OR with siNOTCH4, siSTAT3 or their combination treatments. (n = 5 PDXs). m and o The tumor weight of PDX models of PC-9GR/PC-9OR with siNOTCH4, siSTAT3 or their combination treatments. (n = 5 PDXs) mean ± SD. An unpaired two-sided student t-test was performed in Fig. 6a–d, and 6f–o. Three biologically independent experiments were performed for Fig. 6e. Source data are provided as a Source Data file.

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