Aim
Emodin was found effective in suppressing proliferation of cancer cells including colorectal cancer (CRC), but the mechanisms were still unclear. This study was aimed to investigate the possible mechanism of emodin's anti-CRC effects.
Conclusions
emodin inhibited proliferation of human CRC cells by inducing cell apoptosis by activating ROS/p38/p53/Puma signaling.
Methods
Two most frequently used CRC cell lines, SW480 and SW620, were investigated in this study. Serially diluted emodin solutions were used to incubate CRC cells. siRNAs were used to silence the expressions of p38 and Puma respectively. Intracellular ROS production was detected by DCFH-DA staining; proliferation and apoptosis of CRC cells were assessed by MTT assay and Hoechst staining respectively. Western blotting was applied to evaluate the activation of p38/p53/Puma signaling.
Results
Both in SW480 and SW620 cells, emodin inhibited proliferation by inducing ROS-mediated apoptosis in a concentration-dependent manner. The p38/p53/Puma signaling was also activated after emodin incubation in a concentration-dependent manner. The ROS scavenger NAC, p38 silencing and Puma silencing impaired the anti-proliferation and apoptosis- inducing effects of emodin. Conclusions: emodin inhibited proliferation of human CRC cells by inducing cell apoptosis by activating ROS/p38/p53/Puma signaling.