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Fig. 7 | Journal of Translational Medicine

Fig. 7

From: The BRD4 inhibitor JQ1 suppresses tumor growth by reducing c-Myc expression in endometrial cancer

Fig. 7

JQ1 and BRD4 knockdown suppressed expression of c-Myc and PI3K/AKT/mTOR pathway. A HEC-1A, Ishikawa, RL-95 and An3C cells were treated with DMSO, 0.1 µM, 1 µM and 10 µM JQ1 for 48 h. Protein expressions of BRD4, c-Myc and β-Actin were determined by western blot assay. β-Actin served as the loading control. B The protein bands were quantified using ImageJ software and standardized by the β-Actin protein level. Data shown are mean ± SD from three independent experiments. C HEC-1A and Ishikawa cells were transfected with 150 nM BRD4 siRNA using Lipofectamine 3000. After 72 h, cells were collected for dermining protein expression of BRD4 and c-Myc using western blot assay. β-Actin served as the loading control. D Cells were transfected with c-Myc siRNA. After 72 h, cells were collected for dermining protein expression of c-Myc using western blot assay. E HEC-1A and Ishikawa cells were transfected with BRD4 or c-Myc siRNA. Cell proliferation rate was determined by MTT assay on days 1–5 following transfection. F HEC-1A and Ishikawa cells were transfected with BRD4 siRNA for 72 h. Protein expressions of PI3K, AKT, phosphorylated AKT, mTOR, phosphorylated mTOR and β-Actin were determined by western blot assay. β-Actin served as the loading control. G Pearson correlation between BRD4 and c-Myc genes was performed using cBioPortal and Gene Expression Profiling and Interactive Analysis (GEPIA)

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