Evaluation of curcumin effects on viability and proliferation of CML cell lines
MSc student: Esma Bilajac
Mentor: Assist. Prof. Dr. Mirza Suljagic
Chronic myeloid leukemia (CML) is a myeloproliferative hematological malignancy characterized by constitutive activation of BCR-ABL1 tyrosine kinase (TK) in the majority of patients. The activity of BCR-ABL1 TK further activates a whole cascade of signaling pathways involved in cell proliferation, differentiation and survival. Current treatment options for CML involve the use of TK inhibitors (TKI) improving the patient's complete response. However, resistance to first-generation TKI – imatinib used in CML treatment represents a major issue. The promising treatment option for CML is curcumin. Curcumin has been found to exhibit anti-cancerous effects in various models, including CML, through the regulation of multiple molecular signaling pathways contributing to cancerogenesis. In our study, we have performed a cell viability assay to evaluate the metabolic rate of imatinib-sensitive LAMA84S and K562, as well as imatinib-resistant LAMA84R cell line upon curcumin treatment. Our results indicate a significant time- and dose-dependent decrease of cell viability in both sensitive and resistant CML models following curcumin treatment. Moreover, we have observed a trend in the decreased proliferation rate of K562 and LAMA84R cell lines after curcumin incubation. Preliminary data of Western blot analysis have shown a dose-dependent decrease of key regulators implied in signaling pathways regulating cell survival, proliferation and differentiation in both cell lines, while curcumin treatment has been shown to induce the expression of caspase-3 in the imatinib-resistant model, suggesting the potential curcumin effect on the regulation of apoptosis in CML. Finally, our results represent a promising approach for future preclinical studies of curcumin role in CML models.
