ArticleTranslational oncology2026
ATO alleviates T-cell immunosuppression by inducing apoptosis-associated secretion of IL-2 in FLT3-ITD-mutated acute myeloid leukemia.
Article in Translational oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundArsenic trioxide (ATO) is effective against FLT3-mutant acute promyelocytic leukemia (APL), but its role in non-APL FLT3-ITD-mutant acute myeloid leukemia (AML) remains unclear. This study aims to investigate the mechanistic impact of ATO on FLT3-ITD-mutated AML cells.
methodsThis study utilized the CCK-8 assay, Wright-Giemsa staining, flow cytometry, Western blotting, and colorimetric assays to assess the effects of ATO on cell viability, cell morphology, apoptosis, Ki67 expression, reactive oxygen species (ROS), IL-2 levels, expression of apoptosis-related proteins, and LDH release in MV4-11 and HL-60 cells. Further validation was performed using NAC, PD98059 and LM22B-10. Following T-cell co-culture experiments, interferon-γ (IFN-γ) and granzyme B (GZMB) levels were measured. Differences in IL-2 expression were validated in primary cells from patients with AML.
resultsCompared to HL-60 cells, ATO-treated FLT3-ITD-mutated MV4-11 cells exhibited lower IC50, reduced Ki67 expression, and elevated LDH levels. ATO induced dose- and time-dependent apoptosis in MV4-11 cells, accompanied by increased Cleaved Caspase-3 expression and Bax/Bcl-2 ratio. NAC attenuated ATO-induced ROS accumulation and apoptosis. ATO suppressed extracellular signal-regulated kinase (ERK) phosphorylation in a concentration-dependent manner, which was reversed by LM22B-10 but exacerbated by PD98059. Additionally, ATO enhanced IL-2 secretion in MV4-11 cells, and their conditioned medium elevated IFN-γ and GZMB levels in CD4
conclusionsATO triggers apoptosis in FLT3-ITD-mutated AML cells via ROS/ERK signaling and modulates T-cell activity through IL-2 secretion, suggesting a dual role in tumor suppression and immune regulation. SIGNIFICANCE: This study confirms that ATO is a potential candidate drug for the treatment of FLT3-ITD-mutant AML and provides mechanistic insights into its cytotoxic and immunomodulatory functions.
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