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Published on: January 21, 2012
The nuclear oncoproteins: RB and p53
1Imperial Cancer Research Fund Laboratory of Molecular Genetics, Institute of Child Health, London, UK.
Abstract:
A novel class of oncogene has been recognised whose loss-of-function results in the expression of the malignant phenotype. Two examples of such genes are the human retinoblastoma predisposition gene (RB1) and the gene encoding the cellular protein p53. These genes are thought to regulate and limit normal proliferation of cells and, as a consequence, can suppress tumorigenicity when introduced into transformed cells. They are hence frequently described as 'tumour suppressor genes'. Both RB1 and p53 gene products are bound by various transforming early proteins encoded by the DNA tumour viruses SV40, adenovirus and human papilloma virus. It is thought that they are thus sequestered and rendered inactive. Thus, a coherent model is emerging whereby inactivation, either by mutation of sequestration, of these tumour suppressor genes may contribute to natural and experimental carcinogenic processes.
Insights
Tumor suppressor genes, like RB1 and p53, normally limit cell proliferation. Their inactivation through mutation or viral protein binding can lead to cancer development.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- A novel class of genes, termed tumor suppressors, has been identified.
- These genes regulate normal cell proliferation and can suppress tumor formation.
Purpose of the Study:
- To explore the role of tumor suppressor genes in the development of the malignant phenotype.
- To understand the mechanisms by which tumor suppressor genes are inactivated.
Main Methods:
- The study focuses on the human retinoblastoma predisposition gene (RB1) and the p53 gene.
- It examines the interaction of RB1 and p53 with viral proteins from SV40, adenovirus, and human papilloma virus.
Main Results:
- Loss-of-function of RB1 and p53 leads to the expression of the malignant phenotype.
- Viral oncoproteins bind to RB1 and p53, sequestering and inactivating them.
Conclusions:
- Inactivation of tumor suppressor genes, via mutation or sequestration, is a key step in both natural and experimental carcinogenesis.
- A model is emerging where the loss of tumor suppressor gene function contributes to cancer development.
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