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Transformation by murine and feline sarcoma viruses specifically blocks binding of epidermal growth factor to cells
Abstract:
Normal cells in culture have membrane receptors for epidermal growth factor (EGF); EGF stimulates cells to divide by binding to these receptors. Cells transformed by murine and feline sarcoma viruses rapidly lose the ability to bind EGF, whereas cells transformed by the DNA tumour viruses, polyoma and SV40, or infected with non-transforming RNA tumour viruses have normal levels of functional EGF receptors. The results suggest that a product of the sarcoma virus genome specifically changes cell EGF receptors; the sarcoma gene product may, then, be functionally related to EGF.
Insights
Sarcoma viruses, unlike other tumor viruses, cause cells to lose epidermal growth factor (EGF) receptors. This suggests the sarcoma virus gene product directly impacts EGF receptor function and may be related to EGF itself.
Area of Science:
- Molecular biology
- Cell biology
- Virology
Background:
- Normal cells utilize membrane receptors for epidermal growth factor (EGF) to regulate cell division.
- Epidermal growth factor (EGF) binding to its receptor triggers cellular proliferation.
Purpose of the Study:
- To investigate the effect of different tumor viruses on the epidermal growth factor (EGF) receptor levels in cultured cells.
- To determine if specific viral gene products are responsible for alterations in EGF receptor function.
Main Methods:
- Culturing cells and transforming them with various viruses, including murine and feline sarcoma viruses, polyoma virus, and SV40.
- Assessing the levels and functionality of epidermal growth factor (EGF) receptors in the transformed cells using binding assays.
Main Results:
- Cells transformed by sarcoma viruses exhibited a rapid loss of functional epidermal growth factor (EGF) receptors.
- Cells transformed by DNA tumor viruses (polyoma, SV40) or infected with non-transforming RNA tumor viruses retained normal EGF receptor levels and function.
- These findings indicate a specific mechanism by which sarcoma viruses alter EGF receptor expression or function.
Conclusions:
- A product encoded by the sarcoma virus genome appears to specifically modify cellular epidermal growth factor (EGF) receptors.
- The sarcoma virus gene product may be functionally linked to epidermal growth factor (EGF) signaling pathways.
- This suggests a potential role for the sarcoma gene product in regulating cell growth through interaction with the EGF receptor system.