Extended Data Fig. 6: HELDR facilitates KAT7 gene expression through recruiting p300 to the KAT7 gene promoter.
From: An EGFR co-amplified lncRNA HELDR promotes glioblastoma malignancy through KAT7-driven gene programs
a, IB for KAT7 protein expression in GSC34 and GSC11 cells with or without HELDR KD. b, IB of KAT7 in GSCs with or without EGFR KD or treatment with the EGFR inhibitor erlotinib. c-e, Representative images of HELDR smFISH with IF for KAT7 or EGFR in GSCs (representative of 50 cells). Arrow: HELDR. f-h, Representative HELDR smFISH with IF for KAT7 or EGFR in human GBM tissue (representative of 7 patients). Arrow: HELDR. i, Gene correlation analysis of HELDR and KAT7 genes in TCGA (n = 169) and CPTAC (n = 91) GBM samples. j, Correlation analysis of RNA-seq data for EGFR RNA in relation to KAT7 in GBM of indicated datasets (TCGA, n = 169; CPTAC, n = 91; NU, n = 47). k, Images of smFISH (HELDR) and IF (p300) in GSC34 and GSC11 cells (representative of 30 cells). Arrow: HELDR. l, HELDR localization compared between top-50% and bottom-50% p300 intensity regions within each nucleus (n = 30 cells). m, n, ChIP-qPCR. Enrichment of p300 (left) and H3K27ac (right) at the KAT7 gene promoter in GSC34 (n = 3) and GSC11 (n = 3) cells with or without HELDR KD. IgG is a control. o, Sequence logo plot and enrichment of ETS family member-binding motif in HELDR ChIRP-seq. Scale bar, 10 μm. β-actin is a sample processing control in a and b. All blots and qPCR are representative of three independent experiments. Two-sided Spearman’s rank correlation test in i, j, two-sided paired t-test in l, two-sided unpaired t-test in m, n, one-sided cumulative binomial test in o, Data are presented as mean ± s.d. (l-n).
