Abstract
Prostate apoptosis response-4 (Par-4) is a proapoptotic gene that selectively induces cell death in most cancer cells. In addition to the increased percentage of apoptotic cells, caspase-3 activity, and poly (ADP-ribose) polymerase (PARP) cleavage, we demonstrate that elevated expression of Par-4 and nuclear entry resulted in apoptosis of nasopharyngeal carcinoma (NPC) cell lines either in serum deprivation or by ectopic overexpression of Par-4. Moreover, disassociation from the Par-4/Akt complex was correlated with the induced proapoptotic ability of Par-4. Therefore, our data suggest that the cytoplasmic localization and expression level of endogenous Par-4 in NPC cells are not sufficient to augment apoptosis.
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 / genetics
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Apoptosis / physiology*
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Apoptosis Regulatory Proteins / genetics
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Apoptosis Regulatory Proteins / metabolism*
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Blotting, Western
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Caspase 3 / metabolism
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Cell Line, Tumor
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Cell Nucleus / metabolism
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Cell Survival / drug effects
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Cell Survival / genetics
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Cell Survival / physiology
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Culture Media, Serum-Free / pharmacology
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Fluorescent Antibody Technique
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Gene Expression Regulation, Neoplastic / drug effects
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Humans
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Intracellular Fluid / drug effects
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Intracellular Fluid / metabolism*
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Nasopharyngeal Neoplasms / genetics
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Nasopharyngeal Neoplasms / metabolism
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Nasopharyngeal Neoplasms / pathology
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Poly(ADP-ribose) Polymerases / metabolism
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Protein Binding
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Proto-Oncogene Proteins c-akt / metabolism
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Proto-Oncogene Proteins c-bcl-2 / genetics
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Proto-Oncogene Proteins c-bcl-2 / metabolism
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Reverse Transcriptase Polymerase Chain Reaction
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Time Factors
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Transfection
Substances
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Apoptosis Regulatory Proteins
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Culture Media, Serum-Free
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Proto-Oncogene Proteins c-bcl-2
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prostate apoptosis response-4 protein
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Poly(ADP-ribose) Polymerases
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Proto-Oncogene Proteins c-akt
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Caspase 3