Department of Biochemistry and Molecular Biology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kawaramachi-Hirokoji, Kamigyo-ku, Kyoto, 602-8566, Japan.
Sci Rep. 2024 Nov 2;14(1):26418. doi: 10.1038/s41598-024-78221-9.
Venetoclax is a BH3 mimetic that was recently approved for the treatment of acute myeloid leukemia (AML) treatment. However, the effect of venetoclax on AML remains limited, and a novel strategy is required. Here, we demonstrate for the first time that the cytotoxic effect of venetoclax drastically increased when by combined with the naturally occurring flavonoid quercetin. Combined treatment with venetoclax and quercetin caused most of AML KG-1 cells to exhibit a condensed morphology. Cell cycle analysis revealed that the combination strongly induced cell death. Caspase inhibitor blocked this cell death, and the combination induced poly (ADP-ribose) polymerase (PARP) cleavage, indicating that apoptosis was the primary mechanism. These effects were also observed in another AML cell line Kasumi-1 but not in chronic myeloid leukemia (CML) K562 cells. Public data analysis demonstrated that B-cell/CLL lymphoma 2 (Bcl-2) expression is increased in AML cells compared to other malignant tumors, and the survival and the growth of AML cell line depends on Bcl-2. We found that quercetin increased Bcl-2-associated X protein (Bax) expression in KG-1. Our study provides a novel function for quercetin and presents a promising strategy for AML treatment using venetoclax.
维奈托克是一种 BH3 模拟物,最近被批准用于治疗急性髓系白血病(AML)。然而,维奈托克对 AML 的疗效仍然有限,需要一种新的策略。在这里,我们首次证明,当与天然存在的类黄酮槲皮素联合使用时,维奈托克的细胞毒性作用大大增强。维奈托克和槲皮素联合治疗导致大多数 AML KG-1 细胞呈现出浓缩的形态。细胞周期分析显示,该联合强烈诱导细胞死亡。半胱天冬酶抑制剂阻断了这种细胞死亡,并且该联合诱导聚(ADP-核糖)聚合酶(PARP)裂解,表明细胞凋亡是主要机制。这些作用在另一种 AML 细胞系 Kasumi-1 中也观察到,但在慢性髓系白血病(CML)K562 细胞中未观察到。公共数据分析表明,与其他恶性肿瘤相比,AML 细胞中 B 细胞/慢性淋巴细胞白血病 2(Bcl-2)的表达增加,并且 AML 细胞系的存活和生长依赖于 Bcl-2。我们发现槲皮素增加了 KG-1 中的 Bcl-2 相关 X 蛋白(Bax)的表达。我们的研究为槲皮素提供了新的功能,并为使用维奈托克治疗 AML 提供了有前途的策略。