Fig. 3.
HDAC3 and STAT3 regulated the expression of PI3K, p-Akt, Akt, p-mTOR, mTOR, Beclin-1, LC3 and p62 in CT26+ colon cancer cells. The viability of CT26+ cells was detected by CCK8 with RGFP966 treatment (A) and NSC74859 treatment (B). (C) The representative expression of Beclin-1, LC3 and p62 in CT26+ cells treated with RGFP966 and NSC74859, β-actin as the internal control for normalization. Quantitative analysis of Beclin-1 (D), LC3 (E) and p62 (F) proteins in RGFP966 and NSC74859 treated groups. (G) The representative expression of PI3K, p-Akt, Akt, p-mTOR, mTOR, p-STAT3, STAT3 and HDAC3 in CT26+ colon cells treated with RGFP966 and NSC74859, β-actin as the internal control for normalization. Quantitative analysis of PI3K (H), p-Akt/Akt (I), p-mTOR/mTOR (J), HDAC3 (K) and p-STAT3/STAT3 (L) in RGFP966 and NSC74859 treated groups. Each experiment was repeated three times, and all the data were presented as mean ± SEM in each case. ANOVA was used when different sets of data were compared. Statistically significant differences between different groups were indicated as *p < 0.05, **p < 0.01 and ***p < 0.001 and ns: no significance.