Acute myeloid leukemia (AML) is a highly heterogeneous malignancy, characterized by the impaired differentiation of myeloid precursors and the rampant clonal proliferation of bone marrow stem cells, which is often accompanied by symptoms such as infection, fever, anemia, and bleeding. AML constitutes approximately 80% of all adult leukemia cases and is distinguished by its high morbidity and mortality rates. Traditional Chinese Medicine (TCM) exhibits distinct characteristics and advantages in the treatment of contemporary hematological diseases, particularly in the management of relapsed and refractory blood diseases, as well as in addressing complications arising from Western medical treatments. This study investigates the therapeutic potential of Bufalin, the active component of Cinobufotalin derived from Bufo toad venom, in the context of AML. Utilizing the K562 cell line, we investigated the mechanism of bufalin through the GSE6347 database and in vitro experiments. Our results indicate that bufalin initially stimulates and subsequently inhibits the JAK-STAT signaling pathway, thereby facilitating apoptosis. Molecular docking with AutoDock Vina suggests that bufalin may induce autophagy by targeting transport proteins. By modulating apoptosis and autophagy via the JAK-STAT pathway, bufalin exhibits a distinctive dual effect on leukemia cells. This study underscores bufalin as a potential therapeutic agent for AML, integrating TCM principles with contemporary molecular techniques. These findings lay the groundwork for further exploration of bufalin's clinical potential and its role as a targeted therapy for modulating cell death in AML.

To Cite This Article: Wu Z, Cui Y, Mao W, Li Y, Memon MA and Lan H, 2024. Bufalin promotes apoptosis and autophagy through the JAK-STAT signaling pathway in myeloid leukemia. Pak Vet J, 44(4): 1142-1152. http://dx.doi.org/10.29261/pakvetj/2024.298