Presentation description

Acute Myeloid Leukemia (AML) is a severe hematopoietic malignancy characterized by rapid disease progression and limited treatment options. This study investigates the role of the F-box protein FBXO25 in AML, focusing on its regulatory influence on cellular processes essential for cancer progression. Using MOLM 13 cells, a model for AML, we performed protein labeling experiments to assess degradation mediated by FBXO25. Transfected cells with FBXO25 plasmids were analyzed, and supernatants were collected at various time points.

Western blot analyses showed that FBXO25 overexpression in MOLM 13 cells resulted in significant changes in protein expression, further underscoring its potential role in leukemia progression. Immunoprecipitation and flow cytometry was employed as well.

The ubiquitin-proteasome system plays a crucial role in protein regulation, with E3 ligases serving as the substrate-recognizing components. F-box proteins, such as FBXO25, are responsible for recognizing approximately 20% of ubiquitinated proteins. Our findings suggest that FBXO25 directs specific proteins for proteasomal degradation, implicating its involvement in AML progression.

Future research will explore the impact of FBXO25 knockdown on apoptosis and proliferation in various AML cell lines and compare its effects with other F-box proteins like FBXO21. Understanding these mechanisms could lead to the development of targeted therapies aimed at modulating FBXO25 activity, ultimately contributing to more effective treatment strategies for AML and other hematopoietic malignancies.