Abstract
p202, an IFN-inducible protein, interacts with several important regulatory proteins, leading to growth arrest or differentiation. In this report, we demonstrate that, in addition to inhibiting in vitro cell growth, p202 can also suppress the tumorigenicity of breast cancer cells in vivo. Furthermore, we found that p202 expression could sensitize breast cancer cells to apoptosis induced by tumor necrosis factor alpha treatment. One possible mechanism contributing to this sensitization is the inactivation of nuclear factor-kappaB by its interaction with p202. These results provide a scientific basis for a novel therapeutic strategy that combines p202 and tumor necrosis factor alpha treatment against breast cancer.
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.
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Apoptosis / physiology*
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Breast Neoplasms / genetics
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Breast Neoplasms / metabolism*
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Breast Neoplasms / physiopathology
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Carrier Proteins / genetics
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Carrier Proteins / physiology*
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Female
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Humans
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Intracellular Signaling Peptides and Proteins*
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NF-kappa B / physiology*
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Neoplasm Proteins / physiology*
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Phenotype
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Phosphoproteins / genetics
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Phosphoproteins / physiology*
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Transfection
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Tumor Cells, Cultured / drug effects
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Tumor Necrosis Factor-alpha / pharmacology*
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Tumor Suppressor p53-Binding Protein 1
Substances
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Carrier Proteins
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Intracellular Signaling Peptides and Proteins
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NF-kappa B
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Neoplasm Proteins
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Phosphoproteins
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TP53BP1 protein, human
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Tumor Necrosis Factor-alpha
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Tumor Suppressor p53-Binding Protein 1