Abstract
Selenium (Se) is an essential micronutrient that functions as a redox gatekeeper through its incorporation into proteins to alleviate oxidative stress in cells. Although the epidemiological data are somewhat controversial, the results of many studies suggest that inorganic and organic forms of Se negatively affect cancer progression, and that several selenoproteins, such as GPXs, also play important roles in tumor development. Recently, a few scientists have examined the relationship between Se and metastasis, a late event in cancer progression, and have evaluated the potential of Se as an anti-angiogenesis or anti-metastasis agent. In this review, we present the current knowledge about Se compounds and selenoproteins, and their effects on the development of metastasis, with an emphasis on cell migration, invasion, and angiogenesis. In the cancers of breast, prostate, colorectal, fibrosarcoma, melanoma, liver, lung, oral squamous cell carcinoma, and brain glioma, there is either clinical evidence linking selenoproteins, such as thioredoxin reductase-1 to lymph node metastasis; in vitro studies indicating that Se compounds and selenoproteins inhibited cell motility, migration, and invasion, and reduced angiogenic factors in some of these cancer cells; or animal studies showing that Se supplementation resulted in reduced microvessel density and metastasis. Together, these data support the notion that Se may be an anti-metastastatic element in addition to being a cancer preventative agent.
Highlights
Unlike other trace elements that interact with proteins non-covalently, selenium (Se) is an essential and unique micronutrient in that it is co-translationally incorporated into polypeptides in the form of the 21st amino acid, selenocysteine (Sec)
Using Lewis lung carcinoma cells, methylseleninic acid (MSA) alone caused a reduction of lung metastasis by 55% in the intramuscular injection model and a 20% decrease in the subcutaneous injection model
MSA, but not SeMet, reduced the expression of urokinase-type plasminogen activator (uPA) and plasminogen activator inhibitor-1 (PAI-1). These findings suggested that MSA may reduce Lewis lung cancer metastasis by inhibiting the entire urokinase plasminogen activator system, which resulted in the decrease of the uPA-mediated extracellular matrix degradation and impaired invasion
Summary
Unlike other trace elements that interact with proteins non-covalently, selenium (Se) is an essential and unique micronutrient in that it is co-translationally incorporated into polypeptides in the form of the 21st amino acid, selenocysteine (Sec). We will present the current knowledge of how selenoproteins and Se supplementation may affect tumor migration, invasion, angiogenesis, and overall metastasis in breast, prostate, colon, melanoma, fibrocarcinoma, glioma, skin, liver, and lung cancers. Selenite in vitro in vitro mammaery endothelial cells carcinogen-induced breast cancer human fibrosarcoma cell, HT1080 apoptosis reduce VEGF [30]. Rat in vitro carcinogen-indeced liver cancer human astrocytoma cell, IPSB-18 reduce angiogenesis, inhibit angiogenic factors reduce MMPs amd EGFR, increase MMP inhibitors [52]. Se-enriched garlic rat carcinogen-induced breast cancer inhibit VEGF, reduce angiogenesis high Se isolated soy proteins mice murine melanoma cell, B16BL6 reduce lung metastasis [54]. GPX3 overexpression reduces primary tumor sizes, eliminates metastasis, and promotes survival inhibit cell migration and invasion
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