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Negation of the cancer-preventive actions of selenium by over-expression of protein kinase Cepsilon and selenoprotein thioredoxin reductase.

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Selenium prevents cancer in some cases but fails to do so in others. Selenium's failure in this respect may be due to the development of resistance to its chemopreventive actions. Selenocompounds induce a variety of cancer-preventive actions in tumor cells, but these actions may be limited by the

Redox regulation of protein kinase C by selenometabolites and selenoprotein thioredoxin reductase limits cancer prevention by selenium.

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The cancer-preventive mechanism of selenium should address the way low concentrations of selenometabolites react with cellular targets without being diffused from the sites of generation, the way selenium selectively kills tumor cells, and the intriguing U-shaped curve that is seen with dietary

Selenoprotein P, as a predictor for evaluating gemcitabine resistance in human pancreatic cancer cells.

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Gemcitabine is a new standard chemotherapeutic agent used in the treatment of pancreatic cancer, but the mechanisms of gemcitabine sensitivity are still controversial. In our study to determine a mechanism that regulates gemcitabine sensitivity, we carried out molecular analysis on the

Selenium and the selenoprotein thioredoxin reductase in the prevention, treatment and diagnostics of cancer.

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Selenium is an essential element that is specifically incorporated as selenocystein into selenoproteins. It is a potent modulator of eukaryotic cell growth with strictly concentration-dependant effects. Lower concentrations are necessary for cell survival and growth, whereas higher concentrations

Effects of selenium status and polymorphisms in selenoprotein genes on prostate cancer risk in a prospective study of European men.

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BACKGROUND Evidence for an association between selenium status and prostate cancer risk is still inconclusive. Anticarcinogenic effects of selenium are supposedly mediated through cellular protective and redox properties of selenoenzymes in vivo. We evaluated the association between serum selenium

The 15kDa selenoprotein and thioredoxin reductase 1 promote colon cancer by different pathways.

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Selenoproteins mediate much of the cancer-preventive properties of the essential nutrient selenium, but some of these proteins have been shown to also have cancer-promoting effects. We examined the contributions of the 15kDa selenoprotein (Sep15) and thioredoxin reductase 1 (TR1) to cancer

Deficiency in the 15-kDa selenoprotein inhibits tumorigenicity and metastasis of colon cancer cells.

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Selenium has cancer-preventive activity that is mediated, in part, through selenoproteins. The role of the 15-kDa selenoprotein (Sep15) in colon cancer was assessed by preparing and using mouse colon CT26 cells stably transfected with short hairpin RNA constructs targeting Sep15. Metabolic (75)Se

Expression of ER-resident selenoproteins and activation of cancer cells apoptosis mechanisms under ER-stress conditions caused by methylseleninic acid

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The aim of this work was to study changes in gene expression levels of 7 ER-resident selenoproteins under ER-stress caused by the action of a selenium-containing compound of organic nature, methylselenic acid using three human cancer cell lines DU 145 (prostate carcinoma), MCF 7 (breast

Evaluation of SEPP1 and Selenoprotein S Gene Polymorphisms (rs7579 and rs34713741) in Relation to Colorectal Cancer Susceptibility in Subset of Iranian Population: A Case-control Study.

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Background

Colorectal cancer (CRC) is rated as the second cause of cancer death worldwide. Selenium (Se) has antioxidant activity and antitumor effect, especially in colon cancer. This important role occurs through selenoproteins. Low Se intake or low plasma Se and selenoproteins

The role of selenoproteins in cancer.

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Evidence has shown that metabolic disorders are common in tumor cells, leading to increased oxidative stress. The increase in the production of reactive oxygen species (ROS) associated with low antioxidant activity has been related to several types of cancer. Selenium, an antioxidant micronutrient,

A possible role for selenoprotein glutathione peroxidase (GPx1) and thioredoxin reductases (TrxR1) in thyroid cancer: our experience in thyroid surgery.

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UNASSIGNED Oxidative stress is responsible for some alterations in the chemical structure and, consequently, in the function of proteins, lipids, and DNA. Recent studies have linked oxidative stress to cancers, particularly thyroid cancer, but the mechanisms remain unclear. Here, we further

Protein Partners of Selenoprotein SELM and the Role of Selenium Compounds in Regulation of Its Expression in Human Cancer Cells.

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The search for potential partners of human SELM in lysates of two cancer cell lines, HT-1080 (fibrosarcoma) and MCF-7 (breast adenocarcinoma), was carried out. Two cytoplasmic actin isoforms-cytoplasmic actin 1 (cytoskeleton β-actin) and cytoplasmic actin 2 (cytoskeletal γ-actin)-were identified as

Selenoproteins reduce susceptibility to DMBA-induced mammary carcinogenesis.

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Selenium is an essential micronutrient in the diet of humans and other mammals. Based largely on animal studies and epidemiological evidence, selenium is purported to be a promising cancer chemopreventive agent. However, the biological mechanisms by which chemopreventive activity takes place are

Arsenic trioxide and auranofin inhibit selenoprotein synthesis: implications for chemotherapy for acute promyelocytic leukaemia.

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OBJECTIVE Arsenicals have been used medicinally for decades to treat both infectious disease and cancer. Arsenic trioxide (As2O3) is effective for treatment of acute promyelocytic leukaemia (APL), yet the mechanism of action of this drug is still widely debated. Recently, As2O3 was shown to inhibit

Differentiated thyroid cancer and selenium supplements for protection of salivary glands from 131I treatment.

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Dear Editor, I read with great interest the article by Son et al about the radioprotective effect of selenium (Se) supplementation for the salivary glands from 131I treatment in patients with differentiated thyroid cancer (DTC). In this study, 8 patients received 300μg of Se (as inorganic sodium

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