Purpose: Colon cancer is a malignant disease with significant mortality. In the present study the anticancer effects of a carbazole alkaloid, Dentatin, were examined against colon cancer cells.
Methods: The colon cancer HT-29 cell line and the normal CCD-18 CO colon cell line were used in the present study. MTT assay was used to check the proliferation rate of the cancer cells. Autophagy was detected by electron microscopy. DNA damage was checked by alkaline comet assay. Cell cycle analysis was performed by flow cytometry. Cell migration was monitored by wound healing assay. Protein expression was checked by western blot analysis.
Results: The results showed that Dentatin inhibited the growth of HT-29 cancer cells in a concentration-dependent manner and with IC50 of 25 µM. However, the IC50 of Dentatin against the normal CCD-18CO colon cells was four times higher (ie.,100 µM). Dentatin inhibited the proliferation of the HT-29 cancer cells by triggering S-phase arrest. This was also accompanied with increase in the expression of cyclin D1 and decrease in the expression of Cyclin A and B1. Moreover, Dentatin also induced autophagy in the HT-29 cells which was associated with upregulation of LC3 II and downregulation of Beclin-1 expression. Comet assay revealed that Dentatin induced DNA damage in the HT-29 cells. Dentatin also significantly inhibited the migration of the HT-29 cells. Finally the effects of Dentatin were examined on the JAK/STAT signalling pathway and it was found that Dentatin inhibited this pathway.
Conclusion: Dentatin may prove to be an essential lead molecule for the management of colon cancer.
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