Fig. 4 | Scientific Reports

Fig. 4

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

Fig. 4

LKB1-p38 MAPK signaling contributed to WMJ-J-09-mediated p21 and survivin regulation. (A) Immunoblot result of p38MAPK phosphorylation in HCT116 cells exposed to WMJ-J-09. (B, C) Immunoblot result of p21 (B) and survivin (C) expression in WMJ-J-09-stimulated HCT116 cells with or without p38 inhibitor III (D) Immunoblot result of LKB1 phosphorylation in HCT116 cells exposed to WMJ-J-09 for indicated periods. (E) Immunoblot results from the effects of LKB1 siRNA or negative control siRNA on p38MAPK and p53 phosphorylation elicited by WMJ-J-09. (F) Immunoblot result of the effects of LKB1 siRNA or negative control siRNA on WMJ-J-09-modulated p21 and survivin expression in HCT116 cells. Each band intensity was quantified, and total α-tubulin levels normalized the fold changes of LKB1, p21, and survivin; total p53 levels normalized that of p53 phosphorylation; total p38MAPK levels normalized that of p38MAPK phosphorylation; total LKB1 levels normalized that of LKB1 phosphorylation. 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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