Abstract
p150, product of the SALL2 gene, is a binding partner of the polyoma virus large T antigen and a putative tumor suppressor. p150 binds to the nuclease hypersensitive element of the c-MYC promoter and represses c-MYC transcription. Overexpression of p150 in human ovarian surface epithelial cells leads to decreased expression, and downregulation to increased expression, of c-MYC. c-MYC is repressed upon restoration of p150 to ovarian carcinoma cells. Induction of apoptosis by etoposide results in recruitment of p150 to the c-MYC promoter and to repression of c-MYC. Analysis of data in The Cancer Genome Atlas shows negative correlations between SALL2 and c-MYC expression in four common solid tumor types.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Antineoplastic Agents, Phytogenic / pharmacology
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Base Sequence
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Cell Line, Tumor
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DNA-Binding Proteins
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Etoposide / pharmacology
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Gene Expression Regulation, Neoplastic
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Genes, Tumor Suppressor*
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Humans
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Molecular Sequence Data
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Neoplasms / genetics
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Neoplasms / metabolism
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Promoter Regions, Genetic
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Protein Binding
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Proto-Oncogene Proteins c-myc / genetics*
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Proto-Oncogene Proteins c-myc / metabolism
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Transcription Factors / genetics*
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Transcription Factors / metabolism
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Transcription, Genetic*
Substances
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Antineoplastic Agents, Phytogenic
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DNA-Binding Proteins
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MYC protein, human
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Proto-Oncogene Proteins c-myc
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SALL2 protein, human
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Transcription Factors
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Etoposide