Department of Clinical Biochemistry, Faculty of Health Sciences, Ben-Gurion University of the Negev, Petakh Tikva, Israel.
Cancer Biol Ther. 2011 Feb 1;11(3):317-29. doi: 10.4161/cbt.11.3.14098.
1α,25-dihydroxyvitamin D3 (1,25D) is a powerful differentiation agent, which has potential for treatment of acute myeloid leukemia (AML), but induces severe hypercalcemia at pharmacologically active doses. We have previously shown that carnosic acid (CA), the polyphenolic antioxidant from rosemary plant, markedly potentiates differentiation induced by low concentrations of 1,25D in human AML cell lines. Here, we demonstrated similar enhanced differentiation responses to the 1,25D/CA combination in primary leukemic cells derived from patients with AML, and determined the role of the Nrf2/antioxidant response element (Nrf2/ARE) pathway in these effects using U937 human monoblastic leukemia cells as the model. CA strongly transactivated the ARE-luciferase reporter gene, induced the ARE-responsive genes, NADP(H)-quinone oxidoreductase and the γ-glutamylcysteine synthetase heavy subunit, and elevated cellular glutathione levels. Interestingly, 1,25D potentiated the effects of CA on these activities. Stable transfection of wild-type (wt) Nrf2 resulted in the enhancement, while transfection of dominant-negative (dn) Nrf2 produced suppression of differentiation induced by the 1,25D/CA combination and, surprisingly, by 1,25D alone. These opposite effects were associated with a corresponding increase or decrease in vitamin D receptor and retinoid X receptor-α protein levels, and in vitamin D responsive element transactivation. Cells transfected with wtNrf2 and dnNrf2 also displayed opposing changes in the levels of the AP-1 family proteins (c-Jun and ATF2) and AP-1 transcriptional activity. Pretreatment with AP-1 decoy oligodeoxynucleotide markedly attenuated the differentiation in wtNrf2-transfected cells, suggesting that the pro-differentiation action of Nrf2 is mediated by functional AP-1. Our findings suggest that the Nrf2/ARE pathway plays an important part in the cooperative induction of myeloid leukemia cell differentiation by 1,25D and a plant polyphenol.
1α,25-二羟维生素 D3(1,25D)是一种有效的分化剂,具有治疗急性髓系白血病(AML)的潜力,但在药理活性剂量下会引起严重的高钙血症。我们之前已经表明,迷迭香植物中的多酚抗氧化剂迷迭香酸(CA)可显着增强低浓度 1,25D 在人 AML 细胞系中诱导的分化。在这里,我们证明了在源自 AML 患者的原代白血病细胞中,1,25D/CA 联合也具有类似的增强分化反应,并使用 U937 人单核白血病细胞作为模型确定了 Nrf2/抗氧化反应元件(Nrf2/ARE)途径在这些作用中的作用。CA 强烈地转录激活 ARE-荧光素酶报告基因,诱导 ARE 反应基因,NADP(H)-醌氧化还原酶和γ-谷氨酰半胱氨酸合成酶重亚基,并提高细胞内谷胱甘肽水平。有趣的是,1,25D 增强了 CA 对这些活性的作用。野生型(wt)Nrf2 的稳定转染导致增强,而显性负(dn)Nrf2 的转染则抑制 1,25D/CA 联合以及令人惊讶的是,单独的 1,25D 诱导的分化。这些相反的作用与维生素 D 受体和视黄酸 X 受体-α蛋白水平的相应增加或减少以及维生素 D 反应元件的转录激活有关。转染 wtNrf2 和 dnNrf2 的细胞还显示出 AP-1 家族蛋白(c-Jun 和 ATF2)和 AP-1 转录活性水平的相反变化。AP-1 诱饵寡脱氧核苷酸预处理显着减弱了 wtNrf2 转染细胞的分化,表明 Nrf2 的促分化作用是通过功能性 AP-1 介导的。我们的研究结果表明,Nrf2/ARE 途径在 1,25D 和植物多酚协同诱导髓样白血病细胞分化中起重要作用。