Journal: Genes & Diseases

Article Title: Druggable target ATAD2 enhances the malignant progression and cooperates with E2F1 to up-regulate PDK1 expression in glioma

doi: 10.1016/j.gendis.2025.101810

Figure Lengend Snippet: ATAD2-E2F1 positive feedback loop regulates the expression of PDK1. (A) Volcano plot of differentially expressed genes from RNA-seq analysis of ATAD2 knockdown and control conditions in LN229 cells. (B) Volcano plot of differentially expressed proteins from proteome analysis of ATAD2 knockdown and control conditions in LN229 cells. (C) The Venn diagram illustrates the overlap between the up-regulated and down-regulated mRNAs and proteins. (D) The fold change ranking plot illustrates 20 commonly down-regulated proteins. (E, F) Western blot analysis confirmed that ATAD2 enhances the expression of PDK1. (G, H) Western blot analysis confirmed that E2F1 up-regulates the expression of ATAD2. (I–K) Western blot analysis validated that E2F1 enhances the expression of ATAD2. (L, M) Western blot analysis showed that ATAD2 cooperates with E2F1 to up-regulate the expression of PDK1. (N) The dual luciferase reporter gene assays revealed that ATAD2 and E2F1 synergistically enhance the promoter activity of PDK1. The data are presented as means ± SD. Statistical comparisons were performed using unpaired two-tailed Student's t -test for figures (F), (H), and (K), and one-way ANOVA followed by Tukey's post hoc test for figures (J), (M), and (N). Statistical significance is denoted as follows: ns, not significant; ∗, P < 0.05; ∗∗, P < 0.01; ∗∗∗, P < 0.001; ∗∗∗∗, P < 0.0001.

Article Snippet: The primary antibodies used for IHC were specific for the following proteins: ATAD2 (CST, cat# 50563, 1:50), Ki67 (Abcam, cat# ab15580, 1:2000), E2F1 (Proteintech, cat# 66515-1-Ig, 1:50), and PDK1 (Proteintech, cat# 18262-1-AP, 1:100).

Techniques: Expressing, RNA Sequencing, Knockdown, Control, Western Blot, Luciferase, Activity Assay, Two Tailed Test

Journal: Genes & Diseases

Article Title: Druggable target ATAD2 enhances the malignant progression and cooperates with E2F1 to up-regulate PDK1 expression in glioma

doi: 10.1016/j.gendis.2025.101810

Figure Lengend Snippet: The clinical significance of the ATAD2-E2F1-PDK1 axis in glioma. (A, B) Analysis using the GlioVis database showed a positive correlation between the expressions of ATAD2, E2F1, and PDK1, as determined by the Spearman correlation test. (C) Representative cases showed the expression of E2F1 and PDK1 in glioma clinical specimens with low and high expression of ATAD2. Scale bar: 100 μm. (D) Spearman's correlation analysis of ATAD2, E2F1, and PDK1 expression levels in glioma clinical specimens. (E) Kaplan–Meier analysis and log-rank test of survival rates across distinct co-expression groups of ATAD2, E2F1, and PDK1 in the CGGA cohort. P values were adjusted for multiple group comparisons using the Bonferroni method. (F) Graphical diagram illustrating that ATAD2 promotes glioma progression and synergizes with E2F1 to increase PDK1 expression. The figure was created using Figdraw ( www.figdraw.com ). Statistical significance is denoted as follows: ∗∗∗, P < 0.001.

Article Snippet: The primary antibodies used for IHC were specific for the following proteins: ATAD2 (CST, cat# 50563, 1:50), Ki67 (Abcam, cat# ab15580, 1:2000), E2F1 (Proteintech, cat# 66515-1-Ig, 1:50), and PDK1 (Proteintech, cat# 18262-1-AP, 1:100).

Techniques: Expressing