Abstract
A model system is proposed to investigate, at the molecular level, the pathways of tumor suppression. As a tool for the selection of cells with a suppressed phenotype, we used the H-1 parvovirus that preferentially kills various neoplastic cells. From the human K562 leukemia cells, we isolated a clone, KS, that is resistant to the cytopathic effect of the H-1 virus and displays a suppressed malignant phenotype. The suppressed malignancy and the cellular resistance to H-1 killing appear to depend on the activity of wild-type p53. Whereas the KS cells express wild-type p53, the protein is undetectable in the parental K562 cells. Experiments with p53 mutants suggest that wild-type p53, in its functionally intact state, contributes to the resistance against the cytopathic effect of H-1 parvovirus.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Antigens, CD / analysis
-
Base Sequence
-
Blotting, Western
-
Cell Survival
-
Clone Cells
-
DNA, Viral / analysis
-
DNA, Viral / genetics
-
Electrophoresis, Gel, Two-Dimensional
-
Genes, Tumor Suppressor*
-
Genes, p53*
-
Humans
-
Leukemia, Myelogenous, Chronic, BCR-ABL Positive
-
Methionine
-
Molecular Sequence Data
-
Molecular Weight
-
Neoplasm Proteins / biosynthesis
-
Neoplasm Proteins / isolation & purification
-
Oligodeoxyribonucleotides
-
Parvoviridae / genetics*
-
Phenotype
-
Polymerase Chain Reaction
-
Suppression, Genetic*
-
Tumor Cells, Cultured
-
Tumor Suppressor Protein p53 / biosynthesis
-
Tumor Suppressor Protein p53 / isolation & purification
Substances
-
Antigens, CD
-
DNA, Viral
-
Neoplasm Proteins
-
Oligodeoxyribonucleotides
-
Tumor Suppressor Protein p53
-
Methionine