Life sciences · 2020
Down-regulating NQO1 promotes cellular proliferation in K562 cells via elevating DNA synthesis.
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Xiao Fei-Yan, Jiang Zhi-Ping, Yuan Fang, Zhou Fang-Jiao, Kuang Wei, Zhou Gan, Chen Xiao-Ping, Liu Rong, Zhou Hong-Hao, Zhao Xie-Lan, Cao Shan
Аннотация
BACKGROUND: NQO1 protein acts as a cellular protective system, on account of its role as a quinone reductase and redox regulator. Nonetheless, new NQO1 roles are emerging-including its regulation of the cellular proliferation of many tumor cells-and this enzyme has been found to relate to the incidence of various diseases, including chronic myeloid leukemia. However, the mechanisms through which NQO1 influences leukemia progression remain unclear.
MARTIAL AND METHODS: The current study looks to name NQO1 as a novel molecular target that modulates DNA synthesis and chronic myeloid leukemia growth.
RESULTS AND CONCLUSION: Our results indicate that the frequency of the T allele of NQO1 polymorphism in chronic myeloid leukemia patients is higher than that among healthy East Asian individuals (0.492 vs. 0.419) and much higher than the average level of the general population (0.492 vs. 0.289) (1000 Genomes). Functionally, NQO1 knockdown increases the protein expression of the TOP2A and MCM complex, and consequently promotes DNA synthesis and K562 cell growth. NQO1 knockdown also promotes tumorigenesis in a xenograft model. NQO1 overexpression, on the other hand, was found to have the opposite effects.
SIGNIFICANCE: Our results show that NQO1 downregulation promotes K562 cellular proliferation via the elevation of DNA synthesis.
MARTIAL AND METHODS: The current study looks to name NQO1 as a novel molecular target that modulates DNA synthesis and chronic myeloid leukemia growth.
RESULTS AND CONCLUSION: Our results indicate that the frequency of the T allele of NQO1 polymorphism in chronic myeloid leukemia patients is higher than that among healthy East Asian individuals (0.492 vs. 0.419) and much higher than the average level of the general population (0.492 vs. 0.289) (1000 Genomes). Functionally, NQO1 knockdown increases the protein expression of the TOP2A and MCM complex, and consequently promotes DNA synthesis and K562 cell growth. NQO1 knockdown also promotes tumorigenesis in a xenograft model. NQO1 overexpression, on the other hand, was found to have the opposite effects.
SIGNIFICANCE: Our results show that NQO1 downregulation promotes K562 cellular proliferation via the elevation of DNA synthesis.
Предметные рубрики MeSH
AdultAllelesAnimalsAsian PeopleCell Line, TumorCell ProliferationDNA Topoisomerases, Type IIDNA, NeoplasmFemaleGene Expression Regulation, LeukemicHeterograftsHumansK562 CellsLeukemia, Myelogenous, Chronic, BCR-ABL PositiveLeukocytesMaleMiceMice, NudeMiddle AgedNAD(P)H Dehydrogenase (Quinone)Poly-ADP-Ribose Binding ProteinsPolymorphism, GeneticRNA, Small InterferingSignal Transduction