Selenoprotein‐P is down‐regulated in prostate cancer, which results in lack of protection against oxidative damage

Gonzalez-Moreno, Oscar; Boqué, N. Bultó; Redrado, Miriam; Milagro, Fermı́n I.; Campión, Javier; Endermann, Tobias; Takahashi, Kazuhiko; Saito, Yoshiro; Catena, Raúl; Schomburg, Lutz; Calvo, Alfonso

doi:10.1002/pros.21298

Cited by 35 publications

(27 citation statements)

References 53 publications

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“…A recent study showed a downregulation of SepP in PCa which leads to decreased cellular protection against oxidative damage [24]. Our data demonstrated that compared to control, a marked up-regulation of SepP occurs in all the treatment groups except MSA (Figure 6B).…”

Section: Resultssupporting

confidence: 63%

“…A recent study demonstrated that SepP is reduced in 60.8% of human prostate tumors as compared to benign prostates [24]. Our data shows marked increase in SepP expression in γT1 and MSA + γT1 groups, favoring lower dose of γT over a higher dose.…”

Section: Discussionsupporting

confidence: 56%

“…qRT-PCR was performed with SYBR Premix Ex Taq II (Clontech Laboratories, Inc.) with pooled first strand cDNA and appropriate forward and reverse primers. The following primers were used: Bax, F:5'-AGAGGATGATTGCCGCCGT-3' and R:5-CAACCACCCTGGTCTTGGATC-3' [30]; Bcl2, F:5'-CATGTGTGTGGAGAGCGTCAA -3' and R:5'-ACAGTTCCACAAAGGCATCCC-3' [30]; Bad, F:5'-CCGAGTGAGCAGGAAGACTC-3' and R: 5'-GGTAGGAGCTGTGGCGACT-3' [38]; ApoE, F:5'-TGCTCAGCTCCCAGGTCAC-3' and R:5'-GCCTTCAACTCCTTCATGGTCT-3' [39]; SepP, F:5'-GTCTTCCCTCAGTAAGTACT-3' and R:5'-CTTCTCCACATTGCTGAGGT-3' [24]; Nrf2, F:5'-TGAAGCTCAGCTCGCATTGATCC-3' and R:5'-AAGATACAAGGTGCTGAGCCGCC-3' [17]; GAPDH, F:5'-TCCTCTGACTTCAACAGCGACAC-3' and R:5'-CACCCTGTTGCTGTAGCCAAATTC-3' [40]. The qRT-PCR assays were performed on the StepOnePlus Real-Time PCR System (Life Technologies Corp.).…”

Section: Methodsmentioning

confidence: 99%

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Methaneseleninic acid and γ-Tocopherol combination inhibits prostate tumor growth in Vivo in a xenograft mouse model

et al. 2014

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Studies have shown that vitamin E and selenium possess antiproliferative effects against prostate cancer (PCa). However, results from the Selenium and Vitamin E Cancer Prevention Trial (SELECT) suggest that vitamin E (α-tocopheryl acetate; 400 mg) and/or selenium (L-selenomethionine; 200 μg) were ineffective against PCa in humans. It is arguable that the selected dose/formulation of vitamin E/selenium were not optimal in SELECT. Thus, additional studies are needed to define the appropriate formulations/dose regimens of these agents. Here, we investigated the effect of methaneseleninic acid (MSA; 41 μg/kg) and/or γ-tocopherol (γT; 20.8 mg/kg or 41.7 mg/kg) in Nu/J mice implanted with 22Rν1 tumors. MSA (41 μg/kg) and γT (20.8 mg/kg) combination was most consistent in imparting anti-proliferative response; resulting in a significant decrease in i) tumor volume/weight, ii) serum PSA, and iii) Ki-67 immunostaining. Further, we observed i) an upregulation of pro-apoptosis Bax and a down-regulation of the pro-survival Bcl2, and ii) an increase in pro-apoptosis Bad. Furthermore, the combination resulted in a modulation of apolipoprotein E, selenoprotein P and Nrf2 in a fashion that favors antiproliferative responses. Overall, our study suggested that a combination of MSA and γT, at lower dose regimen, could be useful in PCa management.

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Section: Resultssupporting

confidence: 63%

Section: Discussionsupporting

confidence: 56%

Section: Methodsmentioning

confidence: 99%

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Methaneseleninic acid and γ-Tocopherol combination inhibits prostate tumor growth in Vivo in a xenograft mouse model

et al. 2014

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“…serum Se and selenoprotein P (SePP) concentrations are reduced in prostate cancer patients and this is correlated with disease severity [13]. This in turn could reduce selenoprotein expression and associated anti-oxidant defense resulting in increased oxidative damage leading to prostate cancer progression [14].…”

Section: Introductionmentioning

confidence: 99%

Polymorphisms in Thioredoxin Reductase and Selenoprotein K Genes and Selenium Status Modulate Risk of Prostate Cancer

et al. 2012

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Increased dietary intake of Selenium (Se) has been suggested to lower prostate cancer mortality, but supplementation trials have produced conflicting results. Se is incorporated into 25 selenoproteins. The aim of this work was to assess whether risk of prostate cancer is affected by genetic variants in genes coding for selenoproteins, either alone or in combination with Se status. 248 cases and 492 controls from an EPIC-Heidelberg nested case-control study were subjected to two-stage genotyping with an initial screening phase in which 384 tagging-SNPs covering 72 Se-related genes were determined in 94 cases and 94 controls using the Illumina Goldengate methodology. This analysis was followed by a second phase in which genotyping for candidate SNPs identified in the first phase was carried out in the full study using Sequenom. Risk of high-grade or advanced stage prostate cancer was modified by interactions between serum markers of Se status and genotypes for rs9880056 in SELK, rs9605030 and rs9605031 in TXNRD2, and rs7310505 in TXNRD1. No significant effects of SNPs on prostate cancer risk were observed when grade or Se status was not taken into account. In conclusion, the risk of high-grade or advanced-stage prostate cancer is significantly altered by a combination of genotype for SNPs in selenoprotein genes and Se status. The findings contribute to explaining the biological effects of selenium intake and genetic factors in prostate cancer development and highlight potential roles of thioredoxin reductases and selenoprotein K in tumour progression.

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“…The presence of the prostate-specific transglutaminase in PCa has been recently reported as a potential antitumour target ). Yet another important finding from this study were proteins reported to be implicated as potential cancer chemoprevention targets also affiliated with poor nutritional status and metabolic syndrome disease (Das et al, 2011;De Nunzio et al, 2011;DeMarzo et al, 2003;Dong, Zhang, Hawthorn, Ganther, & Ip, 2003;Gonzalez-Moreno et al, 2011;Jeronimo et al, 2004;J. Kim et al, 2005;Kuemmerle et al, 2011;Menendez & Lupu, 2007;Nelson et al, 2005;Oh et al, 2006;Sytkowski, Gao, Feldman, & Chen, 2005;Toki et al, 2010;Tsavachidou et al, 2009;Walsh, 2010;C.…”

Section: Prostate Cancer 41 the Quantitative Proteomic Profiling Of mentioning

confidence: 70%

The Discovery of Cancer Tissue Specific Proteins in Serum: Case Studies on Prostate Cancer

Spiros¹,

Paul²

2012

Biomarker

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Selenoprotein‐P is down‐regulated in prostate cancer, which results in lack of protection against oxidative damage

Abstract: Levels of SepP in prostate cells determine basal ROS levels and sensitivity to H(2)O(2)-induced cytotoxicity. Deregulation of SepP during prostate carcinogenesis may increase free radicals, thus promoting tumor development and de-differentiation.

Cited by 35 publications

References 53 publications

Methaneseleninic acid and γ-Tocopherol combination inhibits prostate tumor growth in Vivo in a xenograft mouse model

Methaneseleninic acid and γ-Tocopherol combination inhibits prostate tumor growth in Vivo in a xenograft mouse model

Polymorphisms in Thioredoxin Reductase and Selenoprotein K Genes and Selenium Status Modulate Risk of Prostate Cancer

The Discovery of Cancer Tissue Specific Proteins in Serum: Case Studies on Prostate Cancer

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