Polycomb group (PcG) proteins are epigenetic regulators that reduce tumor suppressor gene expression and promote cancer cell survival. The aim of the present study was to determine whether a bilberry extract (Antho 50) inhibits the expression of PcG proteins in Jurkat cells and, if so, to determine the underlying mechanism. Apoptotic rates and the formation of reactive oxygen species (ROS) were assessed by flow cytometry, and protein expression by Western blotting. Antho 50 induced apoptosis, augmented ROS formation, increased p73, p21 and cleaved caspase-3 expression levels, and decreased those of p-Akt, survivin, PcG proteins, HDACs, DNMT1 and UHRF1. The antioxidant enzyme PEG-catalase prevented the formation of ROS and apoptosis induced by Antho 50 and also by H₂O₂. These findings indicate that Antho 50 promotes apoptosis in Jurkat cells, in part, by decreasing the expression levels of PcG proteins, and, hence, the subsequent PcG proteins-dependent pro-survival events via a redox-dependent mechanism.

聚梳组（PcG）蛋白是表观遗传调节剂，可减少肿瘤抑制基因的表达并促进癌细胞的存活。本研究的目的是确定越桔提取物（Antho 50）是否抑制Jurkat细胞中PcG蛋白的表达，如果是，则确定其潜在机制。通过流式细胞术评估细胞凋亡率和活性氧（ROS）的形成，并通过蛋白质印迹法评估蛋白质的表达。Antho 50诱导细胞凋亡，增加ROS的形成，增加p73，p21和切割的caspase-3表达水平，并降低p-Akt，survivin，PcG蛋白，HDAC，DNMT1和UHRF1的表达。抗氧化酶PEG-过氧化氢酶可防止ROS的形成和Antho 50以及H ₂ O ₂诱导的细胞凋亡。这些发现表明，Antho 50部分地通过降低PcG蛋白的表达水平来促进Jurkat细胞凋亡，并因此通过氧化还原依赖性机制降低随后的PcG蛋白依赖性生存事件。