Cholangiocarcinoma (CCA) classifies as a very deadly disease due to its detrimental effects, late diagnosis, and limited therapeutic options. AKR1B10, cloned from liver cancer, influences cell survival; the usage of epalrestat (EPS) to inhibit this gene results in the apoptosis of carcinoma cells, and utilizing palmitic acid (PA) partly reduces AKR1B10 silence-induced apoptosis. This investigation observed the combined effect of EPS and PA on the apoptosis of cholangiocarcinoma RBE cell. Our data showed that EPS treatment resulted in RBE cell growth inhibition by a concentration dependent and time independent manner. Strangely, the rescue effect of PA in EPSinduced RBE cell did not occur, and combining PA with EPS caused a synergistic effect in RBE cell apoptosis and growth inhibition in which hindering AKR1B10 activity, the loss of MMP, and the production of ROS might be involved; however, this experiment does not answer the questions of how EPS and PA affect AKR1B10 activity, MMP loss and ROS production, and the correlation between AKR1B10 inhibition and MMP loss and ROS production. This investigation concludes that administering EPS and an optimal concentration of PA in the blood by monitoring the amount of PA in the diet is a potential strategy to treat CCA patients.
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