FNBP1 in Chronic Myeloid Leukemia: Spatial Association with BCR-ABL and Potential Implications for Targeted Therapy

Chronic myeloid leukemia (CML) develops as a result of the appearance of the oncoprotein BCR-ABL, which, due to its tyrosine kinase activity, leads to abnormal cellular signal transduction and blast transformation. fNBP1 is a protein involved in cytoskeletal remodeling, endocytosis, phagocytosis, and cell migration, but its functional role in the development of CML is unclear.

to investigate the spatial relationship between fNBP1 and the BCR-ABL oncoprotein in CML cells and to assess the potential involvement of fNBP1 in BCR-ABL-related signaling networks.

The subcellular localization of fNBP1 and BCR-ABL was studied using immunofluorescence staining followed by confocal microscopy in K562 cells. The obtained images were processed and analyzed using fiji software. The bioinformatic analysis of the fNBP1 expression in different cancer types was performed using the GEPIA platform.

The bioinformatic analysis revealed a heterogeneous regulation of the fNBP1 expression in vari- ous malignancies, with the largest increase observed in leukemia. A cytoplasmic punctate distribution of fNBP1 was shown in K562 cells. Partial colocalization between fNBP1 and BCR-ABL was found predominantly in the peripheral cytoplasmic regions.

The observed common spatial distribution of fNBP1 and BCR-ABL enhances the understanding of this protein complex's formation, suggesting a potential role for fNBP1 in CML development.