Activation of NQO1 in NQO1*2 polymorphic human leukemic HL-60 cells by diet-derived sulforaphane

Wu, Joseph M.; Oraee, Ardalan; Doonan, Barbara B.; Pinto, John T.; Hsieh, Tze‐chen

doi:10.1186/s40164-016-0056-z

Cited by 9 publications

(9 citation statements)

References 70 publications

(72 reference statements)

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“…These results are not surprising because NQO1 enzyme is involved in metabolic pathways of carcinogens with imbalanced redox homeostasis (21) . The differences between our distribution of both C and T alleles and those reported in previous studies support the concept that the etiology of ALL in children is related to genetic variability at more than one gene locus and may be related to the balance between the metabolic activation and detoxification processes (22) . Lack of agreement between these studies might be due to differences in the duration of the exposure to the oxidative stress, sample sizes, duration of follow up during treatment strategy as well as the demographic stratification (17) .…”

Section: Discussionsupporting

confidence: 71%

Impact of NQO1 C609T Polymorphism on The Outcome of Childhood Acute Lymphoblastic Leukemia from Zagazig University Hospital; Egypt

Eissa¹,

Zidan²,

Hossein³

et al. 2022

The Egyptian Journal of Hospital Medicine

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Background: The NAD (P) H: quinone oxidoreductase (NQO1) C609T polymorphism has been widely thought to be associated with the risk of acute leukemia. Objective: This case-control study aimed to assess the impact of NQO1 C609T gene polymorphism in childhood acute lymphoblastic leukemia (ALL). Patients and Method:The study was carried out on one hundred de novo ALL children and one hundred apparently healthy children. Routine genotyping of NQO1C609T gene polymorphism by PCR-RFLP was done for all subjects. Results: No statistically significant difference was observed between the patient group and control group as regards wild and polymorphic genotypes. However, there was a significant difference between ALL patients with wild and polymorphic genotypes regarding their immunophenotyping diagnosis (P=0.02) and FAB classification (P=0.01). There was also a significant difference between ALL patients with wild and polymorphic genotypes regarding their response to treatment. The complete remission in the wild genotype (CC) was 69.2% while in polymorphic genotypes (TT & CT) was 29.4% (P<0.05). Conclusion:The polymorphic genotype forms of the NQO1 C609T (CT and TT) are associated with decreased response to treatment.

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Section: Discussionsupporting

confidence: 71%

Impact of NQO1 C609T Polymorphism on The Outcome of Childhood Acute Lymphoblastic Leukemia from Zagazig University Hospital; Egypt

Eissa¹,

Zidan²,

Hossein³

et al. 2022

The Egyptian Journal of Hospital Medicine

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“…In addition, Xiao and colleagues tested the samples of peripheral blood or bone marrow specimens obtained from patients suffering from chronic myeloid leukemia and showed that the frequency of loss-of-function mutations of the NQO1 gene was higher than that in healthy individuals. The increased expression of NQO1 was also associated with the suppression of HL-60 cell proliferation [19]. Limonin, which is a secondary metabolite belonging to the tetracyclic triterpenoids, improved the activity of NQO1 in HL-60 cells and promoted apoptosis [54].…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, NQO1 can reduce superoxide in tissues with low levels of superoxide dismutases (SOD) [10]. It was shown that the expression level of the NQO1 gene may be associated with the proliferation of many tumor cells, including brain cancer and leukemia [18][19][20]. NQO1 controls cell proliferation and apoptosis by stabilizing p53 [21].…”

Section: Introductionmentioning

confidence: 99%

Effect of Kaempferol and Its Glycoside Derivatives on Antioxidant Status of HL-60 Cells Treated with Etoposide

et al. 2022

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Kaempferol is a well-known antioxidant found in many plants and plant-based foods. In plants, kaempferol is present mainly in the form of glycoside derivatives. In this work, we focused on determining the effect of kaempferol and its glycoside derivatives on the expression level of genes related to the reduction of oxidative stress—NFE2L2, NQO1, SOD1, SOD2, and HO-1; the enzymatic activity of superoxide dismutases; and the level of glutathione. We used HL-60 acute promyelocytic leukemia cells, which were incubated with the anticancer drug etoposide and kaempferol or one of its three glycoside derivatives isolated from the aerial parts of Lens culinaris Medik.—kaempferol 3-O-[(6-O-E-caffeoyl)-β-d-glucopyranosyl-(1→2)]-β-d-galactopyranoside-7-O-β-d-glucuropyranoside (P2), kaempferol 3-O-[(6-O-E-p-coumaroyl)-β-d-glucopyranosyl-(1→2)]-β-d-galactopyranoside-7-O-β-d-glucuropyranoside (P5), and kaempferol 3-O-[(6-O-E-feruloyl)-β-d-glucopyranosyl-(1→2)]-β-d-galactopyranoside-7-O-β-d-glucuropyranoside (P7). We showed that none of the tested compounds affected NFE2L2 gene expression. Co-incubation with etoposide (1 µM) and kaempferol (10 and 50 µg/mL) leads to an increase in the expression of the HO-1 (9.49 and 9.33-fold at 10 µg/mL and 50 µg/mL, respectively), SOD1 (1.68-fold at 10 µg/mL), SOD2 (1.72-fold at 10–50 µg/mL), and NQO1 (1.84-fold at 50 µg/mL) genes in comparison to cells treated only with etoposide. The effect of kaempferol derivatives on gene expression differs depending on the derivative. All tested polyphenols increased the SOD activity in cells co-incubated with etoposide. We observed that the co-incubation of HL-60 cells with etoposide and kaempferol or derivative P7 increases the level of total glutathione in these cells. Taken together, our observations suggest that the antioxidant activity of kaempferol is related to the activation of antioxidant genes and proteins. Moreover, we observed that glycoside derivatives can have a different effect on the antioxidant cellular systems than kaempferol.

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“…As a consequence of the above findings, we further investigated whether the activation of RNase A-QPN in a low NQO1-expression cell line HEK293T could be enhanced in the presence of sulforaphane, a NQO1 stimulator. 34 As shown in Figure S10, HEK293T cells treated with sulforaphane (1.33 μM) enhanced the intracellular NQO1 level up to 1.6fold compared to the cells without sulforaphane stimulation. Treatment with ROS-TK-12/RNase A-QPN nanoparticle (at a protein concentration of 4.8 μg/mL) resulted in a minimal cytotoxicity on HEK293T cells because of the low NQO1 level in these cells that prevented an effective RNase A-QPN activation (Figure 4b).…”

Section: ■ Results and Discussionmentioning

confidence: 86%

Enzyme-Instructed Activation of Pro-protein Therapeutics In Vivo

et al. 2019

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The selective and temporal control of protein activity in living cells provides a powerful tool to manipulate cellular function and to develop pro-protein therapeutics (PPT) for targeted therapy. In this work, we reported a facile but general chemical approach to design PPT by modulating protein activity in response to endogenous enzyme of disease cells, and its potential for targeted cancer therapy. We demonstrated that the chemical modification of a protein with quinone propionic acid (QPN), a ligand that could be reduced by tumor-cell-specific NAD(P)H dehydrogenase [quinone] 1 (NQO1), was reversible in the presence of NQO1. Importantly, the QPN-modified cytochrome c (Cyt c-QPN) and ribonuclease A (RNase A-QPN) showed NQO1-regulated protein activity in a highly selective manner. Furthermore, the intracellular delivery of RNase A-QPN using a novel type of lipid-based nanoparticles, and subsequent protein activation by cellular NQO1, selectively inhibit cancer cell growth in vitro and effectively suppress tumor growth in vivo. We believe that our approach increases the number of potentially useful chemical tools for reversibly controlling the structure and function of protein using a disease-cell-specific enzyme, opening opportunities in the study of dynamic biological processes and developing precise protein therapeutics.

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Activation of NQO1 in NQO1*2 polymorphic human leukemic HL-60 cells by diet-derived sulforaphane

Cited by 9 publications

References 70 publications

Impact of NQO1 C609T Polymorphism on The Outcome of Childhood Acute Lymphoblastic Leukemia from Zagazig University Hospital; Egypt

Impact of NQO1 C609T Polymorphism on The Outcome of Childhood Acute Lymphoblastic Leukemia from Zagazig University Hospital; Egypt

Effect of Kaempferol and Its Glycoside Derivatives on Antioxidant Status of HL-60 Cells Treated with Etoposide

Enzyme-Instructed Activation of Pro-protein Therapeutics In Vivo

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