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Exploring the diagnostic and prognostic potential of LCFAs' metabolic and biosynthetic pathways in glioblastoma
Ameneh Heydarian1, Behnaz Yazdani2, Hajar Sirous3
1Department of Food Science and Technology, Tehran Medical Sciences, Islamic Azad University Pharmaceutical Sciences Branch, Tehran, Iran.
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 TIM-3, Gal-9, IL-1β, IL-1βR, IL-1βRAP, and NLRP3 genes and IL-1β protein was studied by RT-PCR and ELISA, respectively. Moreover, the effect of Gal-9 on the NF-κΒ signaling pathway was evaluated by western blotting.
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 Gal-9, IL-1B, IL-1BR, and IL-1BRAP were significantly upregulated compared to the control group. The IL-1β concentration increased following Gal-9 treatment in a concentration-dependent manner, while following time its level significantly decreased. Furthermore, Gal-9 slightly increased NF-κΒ phosphorylation.
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-Ιβ production and facilitate AML treatment.
