| Cytotoxic and proapototic activities of imidoselenocarbamate derivatives are dependent on the release of methylselenol. | |
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MedLine Citation:
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PMID: 23043559 Owner: NLM Status: Publisher |
Abstract/OtherAbstract:
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In the search for new molecules with potential antiangiogenic activity, we found that several imidoselenocarbamate derivatives effectively suppressed the expression of vascular endothelial growth factor (VEGF) induced by hypoxia in NCI-H157 tumor cells. Mechanistic studies indicated that these compounds inhibited STAT3 phosphorylation triggered by hypoxia, suggesting that inhibition of STAT3 function may play a role in VEGF inhibition. Moreover, these molecules showed interesting proapoptotic and antiproliferative effects. Both the presence of selenium, but not sulfur, and the nature of the radical substituents were important for activity. Interestingly, under hypoxic conditions several methyl imidoselenocarbamate derivatives released methylselenol, a highly reactive and cytotoxic gas which was responsible for their biological activities. The kinetics of the release of methylselenol by these molecules was highly dependent on the nature of the substituent radicals and correlated with their early proapoptotic activity. Our results support the notion that pharmacological activities reported for methyl imidoselenocarbamate derivatives are dependent on the release of methylselenol. Given the well-known antitumor activities of this compound, imidoselenocarbamate derivatives represent a promising approach to develop new drugs that release methylselenol in a controlled way. |
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Authors:
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Alicia Zuazo; Daniel Plano; Elena Ansó; Elena Lizarraga; Maria Font; Juan J Martinez-Irujo |
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Publication Detail:
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Type: JOURNAL ARTICLE Date: 2012-10-8 |
Journal Detail:
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Title: Chemical research in toxicology Volume: - ISSN: 1520-5010 ISO Abbreviation: Chem. Res. Toxicol. Publication Date: 2012 Oct |
Date Detail:
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Created Date: 2012-10-9 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 8807448 Medline TA: Chem Res Toxicol Country: - |
Other Details:
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Languages: ENG Pagination: - Citation Subset: - |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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