Abstract
In the present study, we demonstrate that ectopic expression of 56-kDa human selenium binding protein-1 (hSP56) in PC-3 cells that do not normally express hSP56 results in a marked inhibition of cell growth in vitro and in vivo. Down-regulation of hSP56 in LNCaP cells that normally express hSP56 results in enhanced anchorage-independent growth. PC-3 cells expressing hSP56 exhibit a significant reduction of hypoxia inducible protein (HIF)-1α protein levels under hypoxic conditions without altering HIF-1α mRNA (HIF1A) levels. Taken together, our findings strongly suggest that hSP56 plays a critical role in prostate cells by mechanisms including negative regulation of HIF-1α, thus identifying hSP56 as a candidate anti-oncogene product.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, Non-P.H.S.
MeSH terms
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Animals
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COS Cells
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Cell Line, Tumor
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Cell Transformation, Neoplastic
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Chlorocebus aethiops
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Down-Regulation
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Humans
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Hypoxia-Inducible Factor 1, alpha Subunit / antagonists & inhibitors
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Hypoxia-Inducible Factor 1, alpha Subunit / genetics
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Hypoxia-Inducible Factor 1, alpha Subunit / metabolism*
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Male
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Mice
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Mice, Inbred ICR
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Mice, SCID
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Prostatic Neoplasms / metabolism
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Prostatic Neoplasms / pathology*
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Protein Binding
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RNA Interference
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RNA, Messenger / metabolism
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Selenium-Binding Proteins / metabolism*
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Transplantation, Heterologous
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Ubiquitin Thiolesterase / metabolism
Substances
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Hypoxia-Inducible Factor 1, alpha Subunit
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RNA, Messenger
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SELENBP1 protein, human
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Selenium-Binding Proteins
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USP20 protein, human
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USP33 protein, human
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Ubiquitin Thiolesterase