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Suppression of tumorigenicity in clones of hamster cells transformed with avian sarcoma virus
1Cancer Research Institute, Slovak Academy of Sciences, Bratislava, Czechoslovakia.
Abstract:
Hamster cells transformed with avian sarcoma virus, which had been selected for resistance to 8-azaguanine, were cloned. Several single cell clones were isolated which differed significantly in their tumorigenicity in comparison to the parental highly tumorigenic cells. The nontumorigenic cell clones contained rescuable avian virus. Both parental and resistant cells possessed transformed phenotype. Comparative studies with parental highly tumorigenic cells and nontumorigenic cell clones failed to detect any difference in the expression of p60src, in this phosphorylation and in phosphokinase activity. The isolated nontumorigenic cells represent cell mutants in which the viral src gene is controlled by a suppressor gene. The cells might be useful for further characterization of a putative antioncogene.
Insights
Researchers identified hamster cell mutants resistant to 8-azaguanine, showing reduced tumorigenicity despite containing avian sarcoma virus. These nontumorigenic cells may harbor a suppressor gene controlling the viral src gene, offering insights into antioncogenes.
Area of Science:
- * Molecular Biology
- * Oncology
- * Virology
Background:
- * Avian sarcoma virus (ASV) transformation of hamster cells leads to a highly tumorigenic phenotype.
- * Selection for resistance to 8-azaguanine can yield cell variants with altered characteristics.
Purpose of the Study:
- * To isolate and characterize hamster cell clones with varying tumorigenicity after ASV transformation and 8-azaguanine selection.
- * To investigate the role of the viral src gene and potential suppressor genes in cell tumorigenicity.
Main Methods:
- * Cloning of ASV-transformed hamster cells selected for 8-azaguanine resistance.
- * Tumorigenicity assays in vivo.
- * Analysis of viral presence and rescuability.
- * Comparative studies of p60src expression, phosphorylation, and phosphokinase activity.
Main Results:
- * Isolation of single-cell clones with significantly reduced tumorigenicity compared to parental cells.
- * Nontumorigenic clones retained rescuable ASV, indicating the virus was present but not driving tumorigenesis.
- * No significant differences were observed in p60src expression, phosphorylation, or activity between tumorigenic and nontumorigenic clones.
Conclusions:
- * Nontumorigenic cell clones represent mutants where the viral src gene's oncogenic potential is suppressed.
- * A suppressor gene likely controls the viral src gene in these resistant cell lines.
- * These cell mutants offer a valuable model for studying putative antioncogenes and their mechanisms.