Potential cancer treatment effects of brusatol or eriodictyol combined with 5-fluorouracil (5-FU) in colorectal cancer cell

Colorectal cancer is among the most frequently diagnosed cancers in patients today. In the treatment of this disease, combination or multicomponent therapy has been identified as a potential method to improve patient response and delay side effects. The aim of this study was to determine the effects on cell viability of commercial Bru and Erio used together with the anticancer drug 5-FU in the human colorectal cancer (CRC) cell line (HT-29 cell line) for the first time, as far as can be determined from available literature at this time. Additionally, the research seeks to study any potential effects on apoptosis. For this purpose, the effects of independent and combined treatments of the aforementioned agents on cell viability were investigated through the MTT experiment. Apoptotic effects were determined by Annexin V/PI and real-time PCR methods. In addition, a cell cycle analysis was used to determine the distribution of cells in the cycle. Data from experiments for 48 h showed that Bru, alone or in combination with 5-FU, is capable of causing an increase in the percentage of apoptotic cells in HT-29 cells compared to those of Erio alone or in combination with 5-FU. A significant increase in the level of bax and caspase-3 apoptotic genes was also detected in combinations of IC50 concentrations of Bru and 5-FU. These findings suggest that unlike Erio, Bru alone or in combination with 5-FU may be useful for increasing the effects of 5-FU used in the treatment of CRC and to provide data on alternative treatment approaches.

Automated summary

This study aimed to investigate the effects of commercial Bru and Erio used in combination with the anticancer drug 5-FU on cell viability and apoptosis in human colorectal cancer cells. Results showed that Bru, alone or in combination with 5-FU, increased apoptosis in HT-29 cells compared to Erio. Additionally, combinations of Bru and 5-FU at IC50 concentrations led to an increase in bax and caspase-3 apoptotic genes.