ArticlePloS one2025
Comparison the impact of IFN-β alone or in combination with vitamin D on critical pathways involved in AML progression.
Article in PloS one, 2025. 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
backgroundAcute myeloid leukemia (AML) is a malignant disorder characterized by the accumulation of immature myeloid cells which can be developed and exacerbated through inflammation. Interferon-β (IFN-β) and vitamin D (Vit D) are known for their immunomodulatory and anti-proliferative effects. Key molecules like IL-1β, Gal-9, β-catenin, and NF-κB play important roles in AML progression. This study examines the effects of IFN-β alone and in combination with Vit D on U937 cell proliferation and the regulation of these key molecules.
methodsCell counting kit-8 (CCK-8) was applied to assess the effect of IFN-β and Vit D on U937 cells proliferation. Real-time PCR was carried out to evaluate the impact of IFN-β and Vit D on IL-1β, IL-10, Gal-9, β-catenin, and NF-κB genes. ELISA was performed to estimate the protein levels of IL-1β and IL-10. Western-blotting was applied to evaluate the NF-κB signaling pathway.
resultsThe proliferation of U937 cells reduced significantly in the presence of IFN-β, while it did not show a remarkable change following treatment with Vit D. IL-1β gene expression was reduced following either IFN-β or Vit D treatment, while IL-10 gene expression underwent a gentl increase following treatment with IFN-β, which was in contrast to Vit D treatment. IFN-β in contrast to Vit D decreased Gal-9 gene expression. β-catenin gene expression increased after IFN-β or Vit D treatment. NF-κB gene expression reduced following either IFN-β or Vit D treatment, except for the highest concentration of Vit D. At protein level, IFN-β and Vit D treatment leads to a reduction of both IL-1β and IL-10 as well as p-NF-κB.
conclusionOur findings suggest that IFN-β effectively inhibits U937 cell proliferation and modulates key inflammatory and immune-related molecules involved in AML pathogenesis. These results highlight IFN-β as a promising agent for targeting critical pathways in AML and suggest a modulatory, but less potent role for Vit D.
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