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A genetic basis for tumour suppression
1Department of Microbiology and Molecular Genetics, California College of Medicine, University of California, Irvine 92717.
Abstract:
The technique of somatic cell hybridization has established the phenomenon of tumour suppression and provided evidence for a genetic basis for suppression. Further refinements aimed at eventually identifying 'tumour suppressor' genes include the use of monochromosome transfer via microcell hybridization. The application of this technique to the study of tumour suppression in tumorigenic HeLa cell x fibroblast hybrids, Wilms' tumour, retinoblastoma and osteosarcoma cells is described. The issue of whether tumour suppression involves a direct effect on expression of activated oncogenes is discussed. Transformation of normal human cells in culture by activated cellular oncogenes is an extremely rare event. This may be due to a relatively greater genomic stability of human cells compared to rodent cells. We describe the use of a spontaneously immortalized human keratinocyte cell line, HaCaT, for studies of the effects of introduction of activated c-Ha-ras oncogene into these cells, with particular reference to tumorigenic conversion.
Insights
Somatic cell hybridization reveals tumor suppression
Area of Science:
- Cancer Genetics
- Cell Biology
- Molecular Oncology
Background:
- Somatic cell hybridization established tumor suppression and its genetic basis.
- Microcell-mediated chromosome transfer is a refinement for identifying tumor suppressor genes.
Purpose of the Study:
- To investigate tumor suppression using microcell hybridization in various cancer cell lines.
- To explore the role of oncogenes in tumor suppression and tumorigenic conversion.
Main Methods:
- Somatic cell hybridization and microcell-mediated chromosome transfer.
- Introduction of activated c-Ha-ras oncogene into HaCaT keratinocytes.
Main Results:
- Demonstrated tumor suppression in hybrids of HeLa cells and fibroblasts.
- Studied tumor suppression in Wilms' tumor, retinoblastoma, and osteosarcoma cells.
- Investigated oncogene-induced transformation in human keratinocytes.
Conclusions:
- Tumor suppression has a genetic basis, potentially involving tumor suppressor genes.
- The interaction between oncogenes and tumor suppressor mechanisms is complex.
- Human cell genomic stability influences oncogene-induced transformation.
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