Evaluation of expression changes of genetic and epigenetic autophagy regulators in chronic myeloid leukemia cells due to epigallocatechin-3-gallate treatment

Purpose: Chronic myeloid leukemia is characterized by the formation and activation of Bcr-Abl1 fusion tyrosine kinase. Discovery of the inhibitor which targets the fusion protein results in a significant increase in survival rates. However the development of resistance to the inhibitor necessitates determining new therapy targets. Autophagy is a remarkable dual target in recent cancer researches. It is usually aimed at inhibition of autophagy because autophagy allows cells to adapt to stress conditions. Epigallocatechin-3-gallate is a basic phytochemical found in green tea. The efficacy of epigenetic regulators, such as microRNAs, is important in the regulation of dietary recommendations as well as in treatment. In this study, it was aimed to investigate the effect of epigallocatechin-3-gallate, a flavanoid, on genetic and epigenetic factors regulating autophagy in chronic myeloid leukemia cells. Materials and methods: microRNAs which are target autophagy-related genes have been identified using appropriate databases. Expression levels of autophagy-related genes and microRNAs targeting these genes were determined using real-time quantitative PCR method in 50 micromolar Epigallocatechin-3-gallate treated K-562 cells. Results: Epigallocatechin-3-gallate treatment resulted in a significant decrease and increase the expression levels of autophagy-related genes and microRNAs targeting these genes in K-562 cells, respectively. Conclusion: In the direction of the results, epigallocatechin-3-gallate was found to cause autophagy inhibition by genetic and epigenetic regulation in chronic myeloid leukemia cells. Considering the dual mechanism of autophagy, this result suggests that epigallocatechin-3-gallate is a chemical that is important for the nutrition of patients as well as its potential to be used as a drug