Analysis of representative cases revealed a clear trend: samples with low ATAD2 expression also exhibited low levels of E2F1 and PDK1, whereas those with high ATAD2 expression showed the opposite trend ( Fig. 7 C).
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Druggable target ATAD2 enhances the malignant progression and cooperates with E2F1 to up-regulate PDK1 expression in glioma.
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