NRH:quinone reductase 2: An enzyme of surprises and mysteries

Vella, F; Ferry, Gilles; Delagrange, Philippe; Boutin, Jean A.

doi:10.1016/j.bcp.2005.09.019

Cited by 134 publications

(123 citation statements)

References 70 publications

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“…In contrast, NQO2 expression is quite variable and dependent, among others, on the species tested. High gene expression, for example, is detected in the skeletal muscle of humans, but not in mouse muscle (58). NQO2 was also found in relatively high levels in normal human liver, while expression of NQO1 was very low, but reverse expression was found in malignant tissues (73).…”

Section: Discussionmentioning

confidence: 98%

“…NQO1 is ubiquitously expressed in physiological and pathological conditions. In malignant conditions, Vella et al found NQO1 in solid tumors of liver, thyroid, adrenal, breast, colon, and non-small cell lung cancers (58). In contrast, NQO2 expression is quite variable and dependent, among others, on the species tested.…”

Section: Discussionmentioning

confidence: 99%

“…The membrane receptors, represented by MT1 and MT2, belong to a G-protein coupled receptor super-family which can bind to a variety of G-proteins (54)(55)(56) and are differentially expressed in melanoma cell lines (24). Cytosolic NRH:quinone oxidoreductase 2 (NQO2, QR2) possesses melatonin binding sites previously described as MT3 receptor (57), differing in this aspect from NAD(P)H:quinone oxidoreductase 1 (NQO1, QR1) (58). Melatonin nuclear receptors, recently identified in keratinocytes, melanocytes and fibroblasts (18) as well as in hair follicles (28), belong to the retinoid orphan receptor subfamily (RZR/ROR).…”

Section: Introductionmentioning

confidence: 99%

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Oncostatic effects of the indole melatonin and expression of its cytosolic and nuclear receptors in cultured human melanoma cell lines

Fischer

Żmijewski²,

Zbytek³

et al. 2006

Int J Oncol

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Abstract.Melatonin has been shown to have oncostatic effects on malignant melanoma in vitro and in vivo. We studied the growth suppressive effects of melatonin over a wide range of concentrations in four melanoma cell lines (SBCE2, WM-98, WM-164 and SKMEL-188) representative for different growth stages and phenotype. Melanoma cells were incubated with melatonin 10 -12 -10 -3 M, and proliferation and clonogenicity was assessed at 12 h and 14 days, respectively. We also determined the expression of cytosolic quinone oxidoreductases NQO1, NQO2 (known as MT3 receptor) and nuclear receptor ROR· by RT-PCR. Melatonin at pharmacological concentrations (10 -3 -10 -7 M) suppressed proliferation in all melanoma cell lines. In SKMEL-188 cells cultured in serum-free media, melatonin at low concentrations (10 -12 -10 -10 M) also slightly attenuated the proliferation. The effects of pharmacological doses of melatonin were confirmed in the clonogenic assay. Expression of NQO1 was detected in all cell lines, whereas NQO2 and nuclear receptor ROR· including its isoform ROR·4 were present only in SBCE2, WM-164 and WM-98. Thus, melatonin differentially suppressed proliferation in melanoma cell lines of different behaviour. The intensity of the oncostatic response to melatonin could be related to the cell-line specific pattern of melatonin cellular receptors and cytosolic binding protein expression.

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Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Oncostatic effects of the indole melatonin and expression of its cytosolic and nuclear receptors in cultured human melanoma cell lines

Fischer

Żmijewski²,

Zbytek³

et al. 2006

Int J Oncol

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“…Moreover, because the prostate stroma seems to be involved in the carcinogenic evolution and progression of prostate epithelial tumor cells, it might be suggested that resveratrol, by targeting QR2, functions as a chemopreventive agent against prostate cancer by its integrative action against prostate cancer cells [13,14] as well as through its growth and gene regulatory control of normal PrSCs. It is noteworthy that QR2 has recently been found to act as a low-affinity melatonin receptor, MT3 [35,36]; this raises the possibility that QR2 might contribute to the prostate cancer chemopreventive activities of melatonin [37][38][39]. We hypothesize that QR2, by binding to melatonin, facilitates and promotes the cytosolic sequestration of androgen receptor, thereby inhibiting cell proliferation and prostate-specific antigen expression.…”

Section: Discussionmentioning

confidence: 94%

Uptake of resveratrol and role of resveratrol-targeting protein, quinone reductase 2, in normally cultured human prostate cells

Hsieh

2009

Asian J Androl

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AbtractResveratrol is a dietary polyphenol espoused to have chemopreventive activity against a variety of human cancer types. We first reported that resveratrol significantly decreases the proliferation of both androgen-dependent and hormone-refractory prostate cancer cells. However, the effects of resveratrol in normal prostate epithelial and stromal cells, particularly with regard to its uptake, subcellular distribution and intracellular targets, have not been investigated. To advance the knowledge on accessibility and cellular disposition of resveratrol in prostate cells, [ 3 H] resveratrol, fractionation of cell extracts into subcellular compartments, Western blot analysis, resveratrol affinity column chromatography and flow cytometry were used to study the uptake and intracellular distribution of resveratrol in normally cultured prostate stromal (PrSCs) and epithelial cells (PrECs). Pretreatment of both PrSCs and PrECs for 2 days with resveratrol modulated its uptake and selectively increased its distribution to the membrane and organelle compartments. Resveratrol affinity column chromatography studies showed differential expression of a previously identified resveratrol-targeting protein, quinone reductase 2 (QR2), in PrSCs and PrECs. Flow cytometric analysis comparing resveratrol-treated and untreated PrSCs showed a large decrease in G 1 -phase and a concomitant increase in S and G 2 /M-phases of the cell cycle. These results suggest that resveratrol suppresses PrSC proliferation by affecting cell cycle phase distribution, which may involve the participation by QR2.

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“…NRH:quinone oxidoreductase 2 (NQO2) has recently been described as an enzyme of surprises and mysteries (Vella et al, 2005). One of the mysteries assumed of NQO2, in contrast to the widely studied homologue NQO1, is that it can use neither NADH nor NADPH as an electron donor.…”

mentioning

confidence: 99%

Reduction of mitomycin C is catalysed by human recombinant NRH:quinone oxidoreductase 2 using reduced nicotinamide adenine dinucleotide as an electron donating co-factor

Jamieson

Tung

Knox³

et al. 2006

Br J Cancer

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NRH:Quinone Oxidoreductase 2 (NQO2) has been described as having no enzymatic activity with nicotinamide adenine dinucleotide (NADH) or NADPH as electron donating cosubstrates. Mitomycin C (MMC) is both a substrate for and a mechanistic inhibitor of the NQO2 homologue NQO1. NRH:quinone oxidoreductase 2 catalysed the reduction of MMC at pH 5.8 with NADH as a co-factor. This reaction results in species that inhibit the NQO2-mediated metabolism of CB1954. In addition, MMC caused an increase in DNA cross-links in a cell line transfected to overexpress NQO2 to an extent comparable to that observed with an isogenic NQO1-expressing cell line. These data indicate that NQO2 may contribute to the metabolism of MMC to cytotoxic species.

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NRH:quinone reductase 2: An enzyme of surprises and mysteries

Cited by 134 publications

References 70 publications

Oncostatic effects of the indole melatonin and expression of its cytosolic and nuclear receptors in cultured human melanoma cell lines

Oncostatic effects of the indole melatonin and expression of its cytosolic and nuclear receptors in cultured human melanoma cell lines

Uptake of resveratrol and role of resveratrol-targeting protein, quinone reductase 2, in normally cultured human prostate cells

Reduction of mitomycin C is catalysed by human recombinant NRH:quinone oxidoreductase 2 using reduced nicotinamide adenine dinucleotide as an electron donating co-factor

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