Interaction of SFPQ with S100A8 and S100A9 in EoL-1 and EoL-1-IR cells
摘要
Hypereosinophilia (HE) is characterized by an abnormal increase of eosinophils in the peripheral blood. It is associated with conditions such as chronic eosinophilic leukemia (CEL) and hypereosinophilic syndrome (HES). Splicing factor proline and glutamine rich (SFPQ) is a multifunctional protein implicated in various cancers. S100A8 and S100A9 are calcium-binding proteins that regulate inflammatory processes.
ObjectivesThis study aimed to investigate the interaction between SFPQ, S100A8, and S100A9 in human eosinophilic leukemia cells (EoL-1), imatinib-resistant EoL-1 (EoL-1-IR), and peripheral blood eosinophils derived from a patient with HES.
ResultsExtracellular stimulation with S100A8 or S100A9 induced apoptosis in EoL-1 and EoL-1-IR cells. SFPQ was identified as an intracellular binding partner of S100A8 and S100A9. In both the nucleus and cytoplasm of EoL-1 and EoL-1-IR cells, S100A8 and S100A9 promoted the formation of SFPQ/S100A8 and SFPQ/S100A9 complexes, respectively, without altering the expression levels of S100A8, S100A9, or SFPQ. Apoptosis induced by S100A8 and S100A9 was positively correlated with the enhanced formation of these heterodimeric complexes in nucleus and cytoplasm. Collectively, these findings suggest that extracellular stimulation with S100A8 or S100A9 enhances the interaction of intracellular S100A8 or S100A9 with SFPQ, thereby contributing to the promotion of apoptosis in EoL-1 and EoL-1-IR cells.
ConclusionThe interaction between SFPQ and S100A8 or S100A9 may play a critical role in promoting apoptosis in eosinophilic leukemia cells, including imatinib-resistant variants.