کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9908974 | 1548427 | 2005 | 13 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Molecular chemoprevention by selenium: A genomic approach
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کلمات کلیدی
azoxymethaneRXRαRT-PCRAOMMSCMSADMBAGHRIGFBP-3LCMMNUapo-ETGFtopoisomerase II alphaNQO1EGR1OPNHMOX1Myc-associated zinc finger protein1,4-phenylenebis(methylene)selenocyanatep-XSCRetinoic acid receptor alphaPCNANAT2MMPFABPMethylnitrosoureaPLAGSTCYP4507,12-Dimethylbenz[a]anthracene - 7،12-Dimethylbenz [a] آنتراسنdhfr - DhfrN-acetyltransferase 2 - N-استیل ترانسفراز 2NAD(P)H:quinone oxidoreductase - NAD (P) H: کینون اکسیدوردوکتازProliferating Cell Nuclear Antigen - آنتیژن هسته ای تکثیر سلولیApolipoprotein-E - آپولیپوپروتئین EOsteopontin - استئوپنتینMethylseleninic acid - اسید متیل سلینینیکtransforming growth factor - تبدیل فاکتور رشدdihydrofolate reductase - دی هیدروفلات ردوکتازTIMP - زمانSOD - سدLung cancer - سرطان ریهProstate cancer - سرطان پروستاتBreast cancer - سرطان پستانColon cancer - سرطان کولونSelenomethionine - سلنمتینیونSelenium - سلنیومSe-methylselenocysteine - سمی متیل سلنوسیستئینSuperoxide dismutase - سوکسوکس دیسموتازCytochrome P450 - سیتوکروم پی۴۵۰phospholipase A - فسفولیپاز Alaser capture microdissection - لیزر ضبط میکرو دیسکسیونmatrix metalloproteinase - ماتریکس متالوپروتئینازTissue inhibitors of metalloproteinases - مهارکننده های متالوپروتئیناز بافتheme oxygenase 1 - همای اکسیژناز 1Reverse transcriptase-polymerase chain reaction - واکنش زنجیره ای واکنش زنجیره ای واکنش زنجیره ایFatty acid binding protein - پروتئین اتصال دهنده اسید چربChemoprevention - پیشگیری شیمیاییearly growth response gene 1 - ژن پاسخ اولیه رشد 1Genomics - ژنومیکMaz - کمیglutathione S-transferase - گلوتاتیون S-ترانسفرازglutathione peroxidase - گلوتاتیون پراکسیدازAndrogen Receptor - گیرنده آندروژنیEstrogen receptor - گیرنده استروژنgrowth hormone receptor - گیرنده هورمون رشد
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
تحقیقات سرطان
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Basic research and clinical chemoprevention trials support the protective role of selenium in cancer prevention but the mechanisms based on the molecular level remain to be fully defined. This mini-review focuses only on the elucidation of the molecular mechanisms of cancer prevention by selenium using the genomics approach; target organs discussed here are breast, prostate, colon and lung. The results described here support the utility of microarray technology in delineating the molecular mechanisms of cancer prevention by selenium. These results are based on studies employing human and rodent cell lines and tissues from animal models ranging from normal to frank cancer. The dose and the form of selenium are determining factors in cancer chemoprevention. The results of the microarray analysis reviewed here indicate that selenium, independent of its form and the target organ examined, alters several genes in a manner that can account for cancer prevention. Selenium can up regulate genes related to phase II detoxification enzymes, certain selenium-binding proteins and select apoptotic genes, while down regulating those related to phase I activating enzymes and cell proliferation. Independent of tissue type, selenium arrests cells in G1 phase of cell cycle, inhibits CYCLIN A, CYCLIN D1, CDC25A, CDK4, PCNA and E2F gene expressions while induces the expressions of P19, P21, P53, GST, SOD, NQO1, GADD153 and certain CASPASES. In addition to those described above, genes such as OPN, which is mainly involved in metastasis and recently reported to be down regulated by selenium, should be considered as potential molecular marker in clinical chemoprevention trials. Collectively, literature data indicate that some of these genes that were altered by selenium are also involved in the development of human cancers described in this review. It appears that androgen receptor status may influence the effect of selenium on gene expression profile in prostate cancer; whether estrogen receptor may influence the effect of selenium on gene expression in breast cancer requires further studies. Knowledge from gene array data in combination with proteomics approaches, using homogenous population of cell types with the aid of laser capture microdissection, may provide an individualized dimension of information on cancer risk and potential targets for its prevention. The molecular (genetic) biomarkers presented in this review will provide the foundation for future studies of the chemopreventive properties of structurally varied selenium compounds.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis - Volume 591, Issues 1â2, 11 December 2005, Pages 224-236
Journal: Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis - Volume 591, Issues 1â2, 11 December 2005, Pages 224-236
نویسندگان
Karam El-Bayoumy, Raghu Sinha,