Antitumor effects of emodin in CACO-2 human colon carcinoma cells are mediated via apoptosis, cell cycle arrest and downregulation of PI3K/AKT signalling pathway.

PURPOSE

Emodin is an important constituent of Rheum emodi, an important medicinal herb. Emodin has been reported to exhibit significant pharmacological potential. Several activities such as anticancer activity have been attributed to emodin. However, the anticancer effects of emodin on colon cancer cells have not been fully studied. Therefore, the present study was designed to investigate the anticancer activity of emodin against the CACO-2 colon carcinoma cells.

METHODS

The anti-proliferative activity of emodin was assessed by MTT assay. Apoptosis, and cell cycle analysis were carried out by flow cytometry using different fluorescent probes. Expression of proteins was examined by western blotting.

RESULTS

The results indicated that emodin reduced the viability of CACO-2 colon cancer cells. The observed IC50 for emodin was 30 μM at 24 hrs of incubation. Furthermore, the anticancer effects of emodin were found to be due to induction of apoptosis. Mitochondrial membrane potential (MMP) determination and Bax/Bcl-2 ratio indicated that emodin-induced apoptosis followed the mitochondrial pathway. Emodin could also trigger cell cycle arrest in CACO-2 colon carcinoma cells in a dose-dependent manner. Evaluation of the effect of emodin in PI3/AKT signalling pathway revealed that emodin could inhibit this signalling cascade indicating the potential of emodin as anticancer drug for the treatment of colon cancer.

CONCLUSION

Emodin exhibited potent anticancer effects in CACO-2 human colon carcinoma cells by inducing apoptosis, cell cycle arrest and inhibition of PI3K/AKT signalling pathway.