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<p>Acute leukemia is an aggressive hematologic malignancy with limited treatment success owing to drug resistance, severe adverse effects, and high costs. Vitexin, a natural compound, demonstrates promising anticancer properties by modulating multiple pathways and inducing apoptosis, while maintaining favorable toxicity profiles. This study examined the pro-apoptotic effects of vitexin on leukemic cell lines (NB-4 and MOLT-4) and patient-derived bone marrow cells, as well as its combined effect with daunorubicin. Cytotoxicity was evaluated using MTT, apoptosis was assessed via Annexin V/PI flow cytometry, and molecular mechanisms were elucidated through in silico bioinformatic, RT-qPCR, and Western blot analyses. Vitexin decreased cell viability in a dose- and time-dependent manner (48&#xa0;hours of IC<sub>50</sub>: 901 µM in NB-4, 929 µM in MOLT-4), with minimal toxicity in normal PBMCs. Synergistic interaction with daunorubicin was confirmed through the combination index. Vitexin elevated apoptosis up to 42.82% by downregulating HIF-1α and upregulating caspase-3 at both transcriptional and translational levels. Patient-derived bone marrow cells, the combination treatment induced the highest apoptosis (22.15% AML, 18.82% ALL). Vitexin induces apoptosis via modulation of HIF-1α/Bcl-2/caspase-3 pathway and potentiates efficacy of daunorubicin, thereby supporting potential as an adjunctive therapeutic in acute leukemia. Further in vivo studies are necessary to elucidate pharmacokinetics and clinical applicability.</p>

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Vitexin induces apoptosis and enhances daunorubicin efficacy in acute leukemia via modulation of the HIF-1α/Bcl-2/caspase-3 pathway

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年12月14日

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  • Chutiphong Jirawatpraphakorn,
  • Dalina Tanyong,
  • Attasak Jaree,
  • Weerapat Owattanapanich

摘要

Acute leukemia is an aggressive hematologic malignancy with limited treatment success owing to drug resistance, severe adverse effects, and high costs. Vitexin, a natural compound, demonstrates promising anticancer properties by modulating multiple pathways and inducing apoptosis, while maintaining favorable toxicity profiles. This study examined the pro-apoptotic effects of vitexin on leukemic cell lines (NB-4 and MOLT-4) and patient-derived bone marrow cells, as well as its combined effect with daunorubicin. Cytotoxicity was evaluated using MTT, apoptosis was assessed via Annexin V/PI flow cytometry, and molecular mechanisms were elucidated through in silico bioinformatic, RT-qPCR, and Western blot analyses. Vitexin decreased cell viability in a dose- and time-dependent manner (48 hours of IC50: 901 µM in NB-4, 929 µM in MOLT-4), with minimal toxicity in normal PBMCs. Synergistic interaction with daunorubicin was confirmed through the combination index. Vitexin elevated apoptosis up to 42.82% by downregulating HIF-1α and upregulating caspase-3 at both transcriptional and translational levels. Patient-derived bone marrow cells, the combination treatment induced the highest apoptosis (22.15% AML, 18.82% ALL). Vitexin induces apoptosis via modulation of HIF-1α/Bcl-2/caspase-3 pathway and potentiates efficacy of daunorubicin, thereby supporting potential as an adjunctive therapeutic in acute leukemia. Further in vivo studies are necessary to elucidate pharmacokinetics and clinical applicability.