Our results, together with the known efficacy of Imiquimod against many tumor entities, suggest that Imiquimod can be a potential alternative therapy to AML. Imiquimod was able to induce apoptosis, as well as to induce cell cycle alteration and upregulation of myeloid differentiation markers on some of the cell lines tested. The activation of particular TLRs on some cell lines can induce growth inhibition and Imiquimod (a TLR 7 agonist) was the most effective agonist in all leukemic cell lines examined. In all experiments, statistical significance was determined by a two-tailed t test. FlowJo software was used to analyze the cytometric data. Differentiation was measured by staining cells with the EuroFlow™ antibody panel for AML and analyzed by flow cytometry. Staining and analysis with a flow cytometer was used to identify cell cycle progression and apoptosis. Proliferation was measured using the CellTiter 96 ® Aqueous One Solution Cell Proliferation Assay (Promega). We investigated the effects of agonists for the ten human TLRs on the proliferation, apoptosis, cell cycle and differentiation of ten different types of myeloid leukemia cell lines (HL-60, U-937, KG-1, KG-1a, K-562, Kasumi-1, EOL-1, NB4, MOLM-13 and HEL). Given that TLR signaling induces hematopoietic cell differentiations this may serve as a novel differentiation therapeutic approach for AML. The antitumoral effects of different Toll-like receptor (TLRs) agonists is mediated by activating immune responses to suppress tumors growth, although TLR ligands may also have a direct effect on tumoral cells.
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January 2023
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