NQO1

Official Full Name

NAD(P)H quinone dehydrogenase 1

Organism

Homo sapiens

GeneID

1728

Background

This gene is a member of the NAD(P)H dehydrogenase (quinone) family and encodes a cytoplasmic 2-electron reductase. This FAD-binding protein forms homodimers and reduces quinones to hydroquinones. This protein's enzymatic activity prevents the one electron reduction of quinones that results in the production of radical species. Mutations in this gene have been associated with tardive dyskinesia (TD), an increased risk of hematotoxicity after exposure to benzene, and susceptibility to various forms of cancer. Altered expression of this protein has been seen in many tumors and is also associated with Alzheimer's disease (AD). Alternate transcriptional splice variants, encoding different isoforms, have been characterized. [provided by RefSeq, Jul 2008]

Synonyms

DTD; QR1; DHQU; DIA4; NMOR1; NMORI;

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Detailed Information

NAD(P)H: Qinionoxedoreducase1 (NQO1), also known as DT-lipoamide dehydrogenase (DT- diaphorase), is a flavin protease containing 274 amino acids. It is expressed in various tissues and organs of mammals, is abnormally expressed in various cancer tissues, and plays an important role in the metabolic detoxification of benzene. NQO1 is an inducible reductase. Various chemical factors such as polycyclic aromatic hydrocarbons, hydroquinones, acrylates, phenolic antioxidants and azo dyes, and environmental factors such as hypoxia can induce their growth.

Functions of NQO1

The chemical protection of NQO1 is closely related to the metabolism of quinone compounds. As a toxic compound, quinone can induce canceration and necrosis of mammalian cells. It exists widely in nature, such as automobile exhaust, tobacco smoke, and even many foods and vitamins (VE, VK, tocopherol). NQO1 can catalyze the conversion of quinone groups to hydroquinone, avoiding nucleophilic damage DNA, reducing the damage to these organelles and genetic material caused by these oxidative active substances, and ensuring the normal physiological function of the body.

NQO1 has been shown to be able to stabilize the expression of wild-type p53 protein and inhibit its degradation through direct protein-protein interactions. Especially when the cells are out of oxidative stress, this stabilizing effect on p53 protein is more prominent. This causes the damaged cells to stop growing in time, undergo repair or undergo apoptosis, block the cell mutation process, and exert their anti-tumor effects. Another study showed that p53 lacks functional NQO1 in cells below the basic level.

NQO1 Figure 1. Schematic summarization of NAD(P)H-quinone oxidoreductase 1 (NQO1) functions. (Pimradasiri Srijiwangsa., et al. 2016)

NQO1 and Cancer Treatment

NQO1 is a key enzyme for the body to protect against active oxygen species and suppress tumors. It can convert estrogen benzoquinone to catechol estrogen, thus limiting the level of estrogen benzoquinone that affects DNA and preventing DNA damage. In estrogen-induced breast cancer, the oxidative stress response produced by the redox cycle between catechol estrogen and estrogen benzoquinone plays an important role. NQO1 not only prevents the estrogen benzoquinone from acting on DNA, but also antagonizes the estrogen-induced oxidative stress response and thus inhibits estrogen-mediated DNA oxidative damage.

Shikonin is a potent inhibitor of the estrogen activation signal in breast cancer cells, and lifetime use of shikonin may reduce the risk of tumor recurrence. In vitro experiments with MCF-7 cell lines confirmed that shikonin can inhibit the growth of estrogen-dependent MCF-7 metastases. Shikonin exerts its chemopreventive effect by activating the detoxifying enzyme NQO1. It activates NQO1 transcription through at least three mechanisms: consumption of ERα receptors; increase in the body's important cell defense mechanism transcription factor NRF2 gene transcription and N2O2 transcriptional activation.

Resveratrol (3,4',5-trihydroxystilbene) prevents malignant tumors by regulating tumor-related pathways, preventing cell proliferation and inducing apoptosis. It can treat and prevent breast cancer by blocking multiple ways of estrogen genotoxicity. Resveratrol induces NQO1 expression and intracellular redistribution, thereby exerting its chemopreventive effect on breast cancer. It can act on estrogen metabolism and the formation of estrogen-DNA adducts, protecting cells from the carcinogenic effects of estrogen metabolites. These studies indicate that inhibiting estrogen signal transduction and activating NQO1 may be a good strategy for preventing estrogen-dependent breast cancer.

References:

Pimradasiri Srijiwangsa., Kesara Na-Bangchang. (2016). Overexpression of nad(p)h:quinone oxidoreductase 1 (nqo1) and genomic gain of the nqo1 locus modulates breast cancer cell sensitivity to quinones. Life Sciences, 145, 57-65.
Wu, X. , Li, X. , Li, Z. , Yu, Y. , You, Q. D. , & Zhang, X. . (2018). Discovery of non-quinone substrates for nad(p)h: quinone oxidoreductase 1 (nqo1) as effective intracellular ros generators for the treatment of drug-resistant non-small cell lung cancer. Journal of Medicinal Chemistry.
Zhang, K. , Cheng, D. , Ma, K. , Wu, X. , Hao, H. , & Jiang, S. . (2018). Nad(p)h:quinone oxidoreductase 1 (nqo1) as a therapeutic and diagnostic target in cancer. Journal of Medicinal Chemistry, acs.jmedchem.8b00124.

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