Abstract
In normal epithelial cells, impaired cell-matrix contact leads to induction of programmed cell death, a process that has been termed 'anoikis'. We investigated the role of p53 and other apoptotic proteins in anoikis in thyroid epithelial cells. Western blot analysis demonstrated that neither p53 nor Bcl-2, Bcl-XL and Bax protein expression changed during anoikis. However, loss of endogenous p53 activity in cells transfected with a dominant-negative mutated p53 inhibited anoikis demonstrating the involvement of p53-dependent processes. The phosphatase inhibitor sodium orthovanadate opposed anoikis when added to the cells within 6 h, suggesting a role for phosphorylated proteins.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Apoptosis / drug effects
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Apoptosis / physiology*
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Cell Adhesion* / drug effects
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Cells, Cultured
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Enzyme Inhibitors / pharmacology
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Epithelial Cells / physiology
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Extracellular Matrix / physiology*
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Humans
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Integrins / physiology
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Phosphoric Monoester Hydrolases / antagonists & inhibitors
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Protein Synthesis Inhibitors / pharmacology
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Proto-Oncogene Proteins / metabolism
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Proto-Oncogene Proteins c-bcl-2 / metabolism
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Thyroid Gland / pathology
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Thyroid Gland / physiology*
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Tumor Suppressor Protein p53 / biosynthesis
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Tumor Suppressor Protein p53 / physiology*
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bcl-2-Associated X Protein
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bcl-X Protein
Substances
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BAX protein, human
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BCL2L1 protein, human
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Enzyme Inhibitors
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Integrins
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Protein Synthesis Inhibitors
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Proto-Oncogene Proteins
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Proto-Oncogene Proteins c-bcl-2
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Tumor Suppressor Protein p53
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bcl-2-Associated X Protein
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bcl-X Protein
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Phosphoric Monoester Hydrolases