Oncogenes transcription factors expressed

In sum, there are oncogenes that reflect every stage of this signaling pathway those that are growth factors mutant growth factor receptors that are always on signal transmission elements that are always on and inappropriate transcription factor expression. In each case, normal controls on the rate of cell division have been overcome. 

A considerable number of transcription factors have reactive cysteine residues, which enable them to respond to the redox conditions in the cell. Since cadmium perturbs redox homeostasis, it can affect this class of transcription factors. If cadmium can displace the tetra-coordinate zinc atoms in zinc finger-containing transcription factors, it will affect them as well. Many of the pathways involving activation and inactivation of transcription factors involve kinases and phosphatases, themselves under the intricate control of calcium fluxes. It is therefore no surprise that cadmium will exert effects on the activity of transcription factors, the activation of proto-oncogenes, and thereby on gene expression (Figure 20.8i and i ). 

Finally, inappropriate expression of nuclear transcription factors can lead to cell transformation. For example, the products of he,fos and myc proto-oncogenes are transcription factors that regulate the expression of proteins that promote progression through the cell cycle. Levels of the Fos and Myc proteins are tightly regulated in normal cells. Uncontrolled expression of these proteins leads to cell proliferation. 

Thurber AE, Douglas G, Sturm EC et al (2011) Inverse expression states of the BRN2 and MITE transcription factors in melanoma spheres and tumour xenografts regulate the NOTCH pathway. Oncogene 30 3036-3048... 

Transcription factor proto-oncogenes that are silent or expressed at low levels in the progenitor cell are activated when placed imder control of potent enhancer elements of genes, which are normally highly expressed. 

Chen A, Xu J, Johnson AC. 2006. Curcumin inhibits human colon cancer cell growth by suppressing gene expression of epidermal growth factor receptor through reducing the activity of the transcription factor Egr-1. Oncogene 25 278-287. 

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