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So what's new with jun?
1Division of Hematology/Oncology, University of Alabama, Birmingham 35294.
Abstract:
Cancer causing oncogenes are found in specific locations within the cell. Although a great deal is known about the function of the transforming genes that reside on the plasma membrane, less is known about the function of the oncogenes that reside in the nucleus. Studies performed over the last three years on the jun and fos oncogenes have taught us a great deal about how these cancer causing genes function in the nucleus. The products of the jun and fos protooncogenes appear to enhance the transcription of specific genes. The proteins form a heterodimer that binds to specific DNA sequences upstream from the start site of transcription and stimulate the production of messenger RNA. Recent data may explain how jun protein becomes transforming. Unlike normal jun protein, transforming jun protein lacks 30 amino acids. These 30 amino acids appear to bind a protein that inhibits the ability of the jun protoncogene to activate gene transcription. The change of cells from normal to transformed may be mediated partially by unrestrained activation of transcription. These findings suggest possible new targets for chemotherapy to inhibit cancer cell growth.
Insights
Nuclear oncogenes like jun and fos enhance gene transcription by forming heterodimers that bind DNA. A 30-amino acid deletion in jun protein may cause uncontrolled transcription, driving cancer cell growth and offering new chemotherapy targets.
Area of Science:
- Molecular Biology
- Oncology
- Gene Regulation
Background:
- Oncogenes are key drivers of cancer, with nuclear oncogenes' functions being less understood than plasma membrane-associated ones.
- The jun and fos proto-oncogenes are nuclear proteins implicated in cancer development.
Purpose of the Study:
- To elucidate the nuclear function of jun and fos proto-oncogenes in gene transcription.
- To investigate the mechanism by which jun protein becomes oncogenic.
Main Methods:
- Analysis of jun and fos proto-oncogene products.
- Investigation of protein-DNA interactions and gene transcription activation.
- Characterization of structural differences between normal and transforming jun proteins.
Main Results:
- Jun and fos proteins form heterodimers that bind specific DNA sequences, enhancing gene transcription and messenger RNA production.
- Transforming jun protein lacks 30 amino acids present in normal jun protein.
- These 30 amino acids appear to bind an inhibitor, preventing jun from activating transcription.
Conclusions:
- Unrestrained transcription activation, potentially mediated by altered jun protein, may drive cellular transformation.
- These findings identify potential therapeutic targets for inhibiting cancer cell proliferation.