Antiangiogenic activity of selenium in cancer chemoprevention: Metabolite-specific effects

Research output: Contribution to journalReview article

69 Citations (Scopus)

Abstract

We review recent data that support a potential antiangiogenic effect of selenium (Se) in the chemoprevention of cancer and data that contrast two pools of Se metabolites, namely, methylselenol vs. hydrogen selenide, that differentially affect proteins and cellular processes crucial to tumor angiogenesis regulation. With regard to tumor angiogenesis, the chemopreventive effect of increased Se intake on chemically induced mammary carcinogenesis has been associated with reduced intratumoral microvessel density and an inhibition of the expression of vascular endothelial growth factor. The in vitro data show that monomethyl Se potently inhibits cell cycle progression of vascular endothelial cells to the S phase, endothelial expression of matrix metalloproteinase-2, and cancer epithelial expression of vascular endothelial growth factor with concentrations giving half-maximal inhibition that are within the plasma range of Se in US adults. The methyl Se-specific activities may therefore be physiologically pertinent for angiogenic switch regulation in early lesions in vivo in the context of cancer chemoprevention, which aims at retarding and blocking the growth and progression of early lesions. We argue for the antiangiogenic action of Se, especially the methyl Se pool of metabolites, as a primary mechanism for preventing avascular lesion growth. Contrary to the currently held paradigm, we speculate that there is a potential role for selenoproteins in regulating the growth and fate of transformed epithelial cells.

Original languageEnglish (US)
Pages (from-to)64-73
Number of pages10
JournalNutrition and cancer
Volume40
Issue number1
DOIs
StatePublished - Jan 1 2001

Fingerprint

Chemoprevention
Selenium
Neoplasms
Vascular Endothelial Growth Factor A
Growth
Selenoproteins
Angiogenesis Inducing Agents
Matrix Metalloproteinase 2
Microvessels
S Phase
Cell Cycle
Carcinogenesis
Breast
Endothelial Cells
Epithelial Cells

All Science Journal Classification (ASJC) codes

  • Medicine (miscellaneous)
  • Oncology
  • Nutrition and Dietetics
  • Cancer Research

Cite this

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abstract = "We review recent data that support a potential antiangiogenic effect of selenium (Se) in the chemoprevention of cancer and data that contrast two pools of Se metabolites, namely, methylselenol vs. hydrogen selenide, that differentially affect proteins and cellular processes crucial to tumor angiogenesis regulation. With regard to tumor angiogenesis, the chemopreventive effect of increased Se intake on chemically induced mammary carcinogenesis has been associated with reduced intratumoral microvessel density and an inhibition of the expression of vascular endothelial growth factor. The in vitro data show that monomethyl Se potently inhibits cell cycle progression of vascular endothelial cells to the S phase, endothelial expression of matrix metalloproteinase-2, and cancer epithelial expression of vascular endothelial growth factor with concentrations giving half-maximal inhibition that are within the plasma range of Se in US adults. The methyl Se-specific activities may therefore be physiologically pertinent for angiogenic switch regulation in early lesions in vivo in the context of cancer chemoprevention, which aims at retarding and blocking the growth and progression of early lesions. We argue for the antiangiogenic action of Se, especially the methyl Se pool of metabolites, as a primary mechanism for preventing avascular lesion growth. Contrary to the currently held paradigm, we speculate that there is a potential role for selenoproteins in regulating the growth and fate of transformed epithelial cells.",
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Antiangiogenic activity of selenium in cancer chemoprevention : Metabolite-specific effects. / Lu, J.; Jiang, C.

In: Nutrition and cancer, Vol. 40, No. 1, 01.01.2001, p. 64-73.

Research output: Contribution to journalReview article

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AU - Jiang, C.

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AB - We review recent data that support a potential antiangiogenic effect of selenium (Se) in the chemoprevention of cancer and data that contrast two pools of Se metabolites, namely, methylselenol vs. hydrogen selenide, that differentially affect proteins and cellular processes crucial to tumor angiogenesis regulation. With regard to tumor angiogenesis, the chemopreventive effect of increased Se intake on chemically induced mammary carcinogenesis has been associated with reduced intratumoral microvessel density and an inhibition of the expression of vascular endothelial growth factor. The in vitro data show that monomethyl Se potently inhibits cell cycle progression of vascular endothelial cells to the S phase, endothelial expression of matrix metalloproteinase-2, and cancer epithelial expression of vascular endothelial growth factor with concentrations giving half-maximal inhibition that are within the plasma range of Se in US adults. The methyl Se-specific activities may therefore be physiologically pertinent for angiogenic switch regulation in early lesions in vivo in the context of cancer chemoprevention, which aims at retarding and blocking the growth and progression of early lesions. We argue for the antiangiogenic action of Se, especially the methyl Se pool of metabolites, as a primary mechanism for preventing avascular lesion growth. Contrary to the currently held paradigm, we speculate that there is a potential role for selenoproteins in regulating the growth and fate of transformed epithelial cells.

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