Galectin-9 induces IL-1β production as a key inflammatory cytokine in the acute myeloid leukemia cell line (U937).

Background and purpose: T-cell immunoglobulin and mucin-domain containing protein-3 (TIM-3)/ galectin-9 (Gal-9)/ autocrine loop in myeloid leukemia stem cells provokes inflammation through the NF-κB signaling pathway, which is influential in the expression of inflammatory factors. Interleukin 1β (IL-1β) is a vital inflammatory cytokine that plays an important role in the proliferation and therapy resistance of acute myeloid leukemia (AML) cells. This study aimed to assess the effect of Gal-9 on IL-1β in the human leukemic U937 cell line. Experimental approach: The U937 cells were cultured in different concentrations of Gal-9. Cell counting kit-8 was used to assess the effect of Gal-9 on human leukemic U937 cell proliferation. Also, its impact on the expression of Findings/Results: U937 cells were expanded in the presence of Gal-9 in a concentration-dependent manner. Following treatment of U937 cells with Gal-9, the gene expression of Conclusion and implications: Gal-9 increased IL-1β level as a critical inflammatory cytokine in the proliferation and resistance of AML cells to therapy. According to this finding, targeting and blocking the TIM-3/Gal-9 autocrine loop can suppress IL-1β production and facilitate AML treatment.