induced colon cancer cells differentiation through JNK/MAPK signalling pathway activation.

[BACKGROUND] Colon cancer is a major health problem with increasing mortality rates worldwide.

[AIM] To evaluate the ability of () to induce differentiation of colon cancer cells to function as normal cells.

[METHODS] The cytotoxic effect of was assessed against Caco cells using the (3-(4,5-dimethylthiazol-2-yl)-2,5-diphe nyltetrazoliumbromide thiazolyl assay. Cell cycle analysis and apoptosis were assessed using Cytell cell system. The total antioxidant (TA), glutathione (GSH), malondialdehyde (MDA) concentrations, and alkaline phosphatase (ALP) activity were also assessed. The c-Jun N-terminal kinases (JNKs) and mitogen-activated protein kinase (MAPK) expressions were evaluated using quantitative real-time polymerase chain reaction.

[RESULTS] There was a significant increase in the cell number treated with (53.85% ± 0.03%), and those treated with sodium butyrate (NaBT) (54.6% ± 0.10%) in sub-G1 phase, compared to the untreated cells (0.78% ± 0.03%, < 0.001). Apoptosis was significantly increased in the Caco cells treated with (49.1% ± 0.14%) compared to those treated with NaBT (27.3% ± 0.10%, < 0.001), and untreated cells (11.1% ± 0.02%, < 0.001). DNA degradation was observed in Caco cells treated with in a dose-dependent manner, where complete degradation occurred at the dose of IC (342.9 μg/mL). induced a significant increase in the TA concentration and GSH, while a significant decrease in the MDA levels ( < 0.001, for all). Also, there was a significant increase in ALP activity in Caco cells (0.53 ± 0.26 U/mL) compared to the control cells (0.05 ± 0.02 U/mL, = 0.045). There was a significant upregulation of JNK and MAPK expression in Caco cells treated with compared to the controls [2.59 ± 0.01 ( < 0.001), and 3.62 ± 0.01 ( < 0.001); respectively].

[CONCLUSION] is a potentially successful therapeutic and differentiating agent for colon cancer.