ArticleMedical principles and practice : international journal of the Kuwait University, Health Science Centre2026
Epigenetic Reactivation of <italic>SOCS-3</italic> and Inhibition of ERK1/2 Underlie Thymoquinone-Induced Apoptosis in a Chronic Myeloid Leukemia Xenograft Model.
Article in Medical principles and practice : international journal of the Kuwait University, Health Science Centre, 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
objectiveThis research aimed to assess thymoquinone (TQ)'s potential to demethylate and re-express the suppressor of cytokine signaling-3 (SOCS-3) in the chronic myeloid leukemia (CML) mice model. SUBJECT AND
methodsA nude mouse model of CML was established, and the apoptotic influence of TQ was identified. TQ's impact on the target gene expressions was examined using real-time quantitative PCR (RT-qPCR), and SOCS-3 methylation was assessed by pyrosequencing. TQ's effects on the extracellular signal-regulated kinase 1 (ERK1) and ERK2 phosphorylation were assessed using Jess Simple Western analysis. Molecular docking of TQ's interaction with the anti-apoptotic proteins was assessed.
resultsTQ exerted a marked hypomethylating influence on SOCS-3 and reduced ERK1/2 phosphorylation level in K562-xenograft tumors. TQ also significantly upregulated the apoptosis-related cysteine peptidase (Caspase-3), BCL-2-interacting mediator of cell death (Bim), p53-upregulated modulator of apoptosis (PUMA), and other apoptotic genes and downregulated B-cell lymphoma 2 (BCL-2), BCL2-like 2 (BCL-w), survivin, and X-linked inhibitor of apoptosis (XIAP) in K562 cells. TQ also exhibited marked inhibitory properties on BCL-2-related gene expressed in fetal liver (BFL-1), B-cell lymphoma-extra large (BCL-xL), myeloid cell leukemia-1 (MCL-1), and BCL-2 proteins. This led to growth inhibition and apoptosis of the K562-tumour xenograft.
conclusionThese results indicate that TQ enhances CML cells' apoptosis by hypomethylating and re-expressing SOCS-3, inhibiting ERK1/2, and modulating the apoptosis-regulator gene expression and by showing consistent interaction with most of the anti-apoptotic proteins, highlighting its potential as a scaffold for designing novel inhibitors to combat CML cells.
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