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 protooncogene 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.
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