Fig. 7
TRIM59-mediated macroH2A1 degradation enhances STAT3 signaling. a Venn diagram shows the overlap of mH2A1-bound sites in the genome in LN229/EGFRvIII cells treated with vehicle (0.1% DMSO), erlotinib (10 μM), or Roscovitine (20 μM) for 16 h using ChIP-Seq. b Heatmap of mH2A1 ChIP-Seq. c Gene ontology analysis of effects of both the treatment of erlotinib and Roscovitine on mH2A1 binding in distance from center of peak (±2 kb) at top five EGFR-driven pathways. d mH2A1 ChIP-Seq peaks at STAT3-targeted genes using IGV (Integrative Genomics Viewer). e ChIP-qPCR of effects of erlotinib or Roscovitine on mH2A1 binding at STAT3-targeted genes. f–h Effects of mH2A1 knockdown in LN229/EGFR and U87/EGFR cells with EGF stimulation. WB for expression of TRIM59, STAT3, and p-STAT3 (f); ChIP-qPCR analysis for STAT3 binding with PIM1 promoter (g); qRT-PCR analysis for STAT3-targeted gene PIM1 transcription (h). i–k Effects of reconstituted TRIM59 WT, S308A, ΔR, or Y218F with or without EGF stimulation. WB for expression of TRIM59, mH2A1, and p-STAT3 (i); ChIP-qPCR analysis for STAT3 binding with PIM1 promoter (j); qRT-PCR analysis for PIM1 transcription (k). Data are representative of three independent experiments with similar results. Data were expressed as means ± SD. **P < 0.01, ***P < 0.001, by two-tailed Student’s t test. Source data are provided as a Source Data file
