Fig 1: Gene Ontology (GO) analysis of 802 craniofacial-specific TFAP2A high confidence peaks (hc-peaks). Bar charts displaying -log10 binomial p-values of enriched mouse single knockout phenotypes with false discovery rate (FDR) < 0.05, human phenotypes with FDR < 0.05 and GO biological processes with FDR < 0.05. Terms relating to orofacial clefting are highlighted in color. Genes associated with these terms in assigned to TFAP2A hc-peaks, based on their proximity, as described in the Methods, are displayed in the boxes.
Fig 2: In silico-predicted TE enhancer-gene contacts show widespread changes in gene expression validated by in vivo CRISPR genome editing.a Differential expression of genes with predicted contacts to MER11 subfamily TEs. Log2 fold change (Log2FC) is shown from RNA-seq data for GP5d vs. HepG2 cells. Red points mark significantly differentially expressed (|Log2FC|> 1.2 and FDR < 0.05), and blue points are insignificant. Log2FCs of ±1.2 and 0 are marked with dashed lines. Boxplots indicate the median (center line), the third and first quartiles (box limits), and 1.5 × IQR above and below the box (whiskers). (n = 80 predicted contacts). b Differential expression of genes with predicted contacts to p53-specific TEs from RNA-seq data between GP5d WT vs. HepG2 cells. Plot elements are like in a. (n = 32 predicted contacts). c Genome browser snapshots of three active MER11B elements with high STARR-seq signal in GP5d cells. Each panel shows the highlighted TE locus with signal tracks in GP5d and HepG2 cells for STARR-seq, ATAC-seq, ChIP-seq for TFAP2A and histone marks, RNA-seq, and predicted enhancer-gene contacts from the ABC analysis. CARD14 in the left panel, HNMT, SPOPL, and SPOPL-DT in the middle panel, and NUDCD1 in the right panel were predicted as gene targets for the MER11B elements. These MER11B elements mostly show STARR-seq activity and canonical epigenetic marks of enhancers in GP5d, likely reflected in the low expression of the target genes in HepG2. d RT-qPCR data showing changes in mRNA expression for genes with predicted contacts to active MER11B elements upon CRISPR-Cas9 mediated deletion of the elements in GP5d cells (GAPDH normalized). Two independent clones with homozygous enhancer deletion were analyzed for MER11B element at chromosome 17 in the vicinity of CARD14 and EIF4A3 (shown in Fig. 6c) and one for MER11B at chromosome 2 flanked by SPOPL, SPOPL-DT and HNMT (shown in Fig. 6c). One heterozygous deletion clone for MER11B at chromosome 8 predicted to regulate NUDCD1 was also tested (shown in Fig. 6c). The figures show mean ± SD values for three technical replicates. Source data are provided as a Source Data file.
Fig 3: TFAP2A could not facilitate or even inhibit LUAD proliferation.A, B Protein expression (up) and transcript levels (down) of TFAP2A for TFAP2A knockdown and overexpression cell models of PC-9 (A) and H1650 (B) (stable gene interference and overexpression by recombinant lentiviruses). C, D Proliferation curves assessed by CCK8 assay during 96 h for TFAP2A knockdown and overexpression cell models of PC-9 (C, knockdown vs. control; D, overexpression vs. control). E, F Plate cloning and statistical analysis for TFAP2A knockdown and overexpression cell models of PC-9 (E, knockdown vs. control; F, overexpression vs. control). G, H Effects on cell cycle progression for TFAP2A knockdown and overexpression cell models of PC-9 (G, knockdown vs. control; H, overexpression vs. control). *p < 0.05; **p < 0.01; ***p < 0.001. N≥3, Data are presented as mean ± standard deviation (SD).
Fig 4: The miR-16 family/TFAP2A/PSG9 axis exhibits clinical effects upon LUAD.A, B The effects of TFAP2A/PSG9 on survival rate in four independent LUAD datasets (GSE30219, GSE31210, GSE41271 and GSE50081) (A, OS rate; B, PFS rate). C, D The influence of miR-16 family/TFAP2A/PSG9 upon survival rate in TCGA-LUAD dataset (C, OS rate; D, PFS rate). E–G The influence of miR-16 family/TFAP2A/PSG9 upon TNM parameters in TCGA-LUAD dataset (E, T parameters: tumor size; F, N parameters: lymph node metastasis; G, M parameters: distant metastasis). *p < 0.05; **p < 0.01; ***p < 0.001.
Fig 5: TFAP2A shows high expression profile in LUAD.A–D TFAP2A transcript levels between normal tissues and tumor tissues in LUAD datasets (GSE10072, GSE32863, GSE43458 and TCGA-LUAD). E IHC staining for TFAP2A protein levels in four paired normal tissues and tumor tissues in LUAD-TMA. F TFAP2A IHC scoring of 127 paired normal and tumor tissues in LUAD-TMA. G Statistical analysis of TFAP2A protein level (IHC scoring) in LUAD-TMA. *p < 0.05; **p < 0.01; ***p < 0.001. Data are presented through boxplots.
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