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Consistent with selectivity of targeting oncogenic growth, MSeA treatment of WT mice did not affect their typical normal glandular structures Fig.
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RNA molecular weight determinations by gel electrophoresis under denaturing conditions, a critical reexamination. As men diagnosed with HG-PIN are at increased risk of developing PCa, this prostate specific conditional Pten KO mouse model recapitulates essential characteristics of human prostate carcinogenesis and is considered clinically relevant for studies of PCa chemoprevention.
Effect of long-term MSeA supplementation on p-Akt and androgen receptor ARsenescence and cellular proliferative index in the anterior prostate of mice in Figure 3.
In fact, the scarce animal efficacy data that existed prior to the initiation of these trials did not support PCa preventive efficacy of SeMet and these negative data were not published in full-length until after SELECT was terminated 9 A new microtechnique for the analysis of the human hepatic microsomal glucosephosphatase system. Short cytoplasmic sequences serve as retention signals for transmembrane proteins in the endoplasmic reticulum. The pathological changes of all lobes of prostate were classified according to Shapell et al.
Null activity of selenium and vitamin e as cancer chemopreventive agents in the rat prostate. In the G6Pase gene of a compound heterozygous patient LLPtwo mutations in exon 2 of one allele and exon 5 of the other allele were identified. The publisher’s final edited version of this article is available free at Cancer Prev Res Phila. As shown in Fig. Unfortunately, recent studies have shown that inhibition of AR signaling by castration or antagonist drugs inadvertently promotes the progression of stable HG-PIN to invasive carcinomas in Pten KO model 19raising concerns for utilization of these androgen deprivation strategies for chemoprevention in high risk men and PCa patients with PTEN deficiency or mutations.
Maintaining and reprogramming genomic androgen receptor activity in prostate cancer. At necropsy, the genitourinary GU tract was collected and weighed. Glycogen storage disease GSD type 1a is an autosomal recessive inborn error of metabolism caused by a deficiency in microsomal glucosephosphatase G6Pasethe key enzyme in glucose homeostasis.
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Distinct effects of methylseleninic acid versus selenite on apoptosis, cell cycle, and protein kinase pathways in DU human prostate cancer cells. Southern blot hybridization analysis using a panel of human-hamster hybrids showed that human G6Pase is a single-copy gene located on chromosome Prostate-specific deletion of the murine Pten tumor suppressor gene leads to metastatic prostate cancer.
C Quantitation of changes from A and B. Mutations in the glucosephosphatase gene that cause glycogen storage disease type 1a. Methyl selenium metabolites decrease prostate-specific antigen expression by inducing protein degradation and suppressing androgen-stimulated transcription.
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For comparison of only 2 groups, student t-test was used. To our best knowledge, this study is the kei in which any form of Se has been tested in the Pten KO PCa mouse model for chemopreventive efficacy. Services Email this article to a friend Alert me when this article is cited Alert me if a correction is posted Alert me when eletters are published Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Download to citation manager Request Permissions.
Identification of le consensus motif for retention of transmembrane proteins in the endoplasmic reticulum. Prostate specific antigen expression is down-regulated by selenium through disruption of androgen receptor signaling. See other articles in PMC that cite the published article.
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DNA methylation and mutation. Prostate pathology of genetically engineered mice: In the Pten KO model, the sustained activation of AKT not only initiates and perpetuates oncogenic signaling and progression pathways, but at the same time induces cellular senescence known as P ten-deficiency I nduced C ellular S enescence PICSwhich acts as a formidable barrier to restrain oncogenic progression to invasive and metastatic disease 16 Journal List J Clin Invest v. We have posited that the failure of SeMet should not be taken to indicate that other Se forms are ineffective for PCa chemoprevention Selenium and prostate cancer prevention: We have previously identified six mutations in the G6Pase gene of glycogen storage disease type 1a patients and demonstrated that these mutations abolished or greatly reduced enzymatic activity of G6Pase, a hydrophobic protein of amino acids.
In the first experiment, we evaluated the effect of 4-week MSeA treatment to identify early biochemical and cellular changes that might correlate and predict its long-term preventive efficacy against HG-PIN growth and tumor progression in Pten KO mice. Open in a separate window.
Support Center Support Center. Role for p53 in selenium-induced senescence. Responses Submit a Letter to the Editor. Abstract Glucosephosphatase G6Pase is the enzyme deficient in glycogen storage disease type 1a, an autosomal recessive disorder. Importantly, these cellular and molecular changes were not observed in the prostate of wild type littermates which were similarly treated with MSeA. Interactions of the system with orthophosphate, inorganic pyrophosphate, and carbamyl phosphate.
Substitution of Arg with amino acids of diverse structures including Lys, a conservative change, yielded mutant G6Pase with no enzymatic activity. This QSP mutation was also detected in all exon 5 subclones five for each patient of two homozygous patients, KB and CB, siblings of the same parents.
Submit your work to JBC. This article has been cited by other articles in PMC.