Fig. 3 | Scientific Reports

Fig. 3

From: The hydroxamate based HDAC inhibitor WMJ-J-09 induces colorectal cancer cell death by targeting tubulin and downregulating survivin

Fig. 3

p53 participates in WMJ-J-09-mediated p21 expression and survivin reduction. (A, B) Immunoblot result of WMJ-J-09-mediated p21 (A) and survivin (B) expression in HCT116 cells. (C, D) Immunoblot result of WMJ-J-09-mediated p21 (C) and survivin (D) expression in p53 wildtype (HCT116) and p53 deficient (HCT116 p53-/-) HCT116 cells. (E) Immunoblot result of p53 phosphorylation and acetylation induced by WMJ-J-09 in HCT116 cells. Each band intensity was quantified, and total α-tubulin levels normalized the fold changes of p21 and survivin; total p53 levels normalized the fold changes of p53 phosphorylation and acetylation. (F) Cells were treated with WMJ-J-09 (5 μM) for 1 or 2 h. ChIP assay was performed as described in the “Methods” Section. Typical traces representative of three independent experiments with similar results are shown. (G) RT-qPCR result of WMJ-J-09-mediated survivin mRNA downregulation. Error bars, mean ± S.E.M. (shown only for independent replicate experiments with n ≥ 4). One-way ANOVA followed by Tukey’s post-hoc test assessed statistical significance (*p < 0.05 compared to the control group).

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