C-myc is a transcription factor that is involved in the strict regulation of the cell cycle. It regulates genes that promote the induction of the cell cycle and it is also involved in apoptosis. The c-myc ¬gene is one of the most commonly activated oncogenes and has been found to be overexpressed in many cancers. Activation of this oncogene may contribute to as many as 100,000 cancer deaths per year in the United States alone (Dang et al., 2006). The discovery that this gene is involved in so many cancers has sparked interest in both the scientific and medical communities. By finding the mechanisms by which this protein can induce cell proliferation, there is a possibility for targeted therapies in cancers that are associated with up-regulation
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C-myc mRNA is very transient in the cell and without positive enforcers to induce translation of this mRNA, very low levels of c-myc are present (Miller et al., 2012).
C-myc can both induce transcription of certain genes and repress transcription of certain genes. Induction of transcription occurs via recruitment of histone acetylases, chromatin modulating proteins, and DNA methyltransferases (Dang et al, 2006). C-myc can also repress transcription through association with Miz1. In its normal function, Miz1 is a transactivating protein that associates with two coactivators, p300 and Npm1. Upon association of c-myc with Miz1, these coactivators get displaced and the Myc/Miz1 complex can recruit DNA methylases and repress transcription (Wiese et al., 2013).
C-myc regulates the cell cycle by repressing and inducing expression of genes that cause progression through it. One main group of genes that c-myc can bind to and regulate expression of are the cyclins and the cyclin-dependent kinases that drive progression through the cell cycle. C-myc was found to bind the E-box of cyclins D1 and D2, CDK4, and cyclin B1 (Dang et al., 2006). CDK4 and both Cyclin D1 and D2 seem to be required for the c-myc transformation to cancer …show more content…
Since c-myc leads to increases in cell proliferation, it follows that the cell would require more protein to be able to function and to produce new daughter cells. C-myc has been shown to regulate genes that encode ribosomal RNAs and proteins that help to synthesize and piece together the ribosomes that function in protein synthesis (van Riggelen et al., 2010). Among these proteins are RNA polymerases I and III, which function in forming the substrate for these ribosomes, mRNA. While the overexpression of c-myc probably leads to a large cell size, it has not been determined if the ribosome biogenesis can lead to the development of neoplastic tissues (Dang et al., 2006).
Another functional group of genes that c-myc regulates the expression of are those that produce cytoskeletal and cell adhesion proteins. The first of these genes to be recognized were those encoding collagen. C-myc consistently repressed these genes across repeated experiments (Dang et al., 2006). N-cadherin is a protein involved in the regulation of hematopoietic stem cells and their movement from the bone marrow out into tissues to mature. C-myc has been found to repress transcription of this gene
C-myc mRNA is very transient in the cell and without positive enforcers to induce translation of this mRNA, very low levels of c-myc are present (Miller et al., 2012).
C-myc can both induce transcription of certain genes and repress transcription of certain genes. Induction of transcription occurs via recruitment of histone acetylases, chromatin modulating proteins, and DNA methyltransferases (Dang et al, 2006). C-myc can also repress transcription through association with Miz1. In its normal function, Miz1 is a transactivating protein that associates with two coactivators, p300 and Npm1. Upon association of c-myc with Miz1, these coactivators get displaced and the Myc/Miz1 complex can recruit DNA methylases and repress transcription (Wiese et al., 2013).
C-myc regulates the cell cycle by repressing and inducing expression of genes that cause progression through it. One main group of genes that c-myc can bind to and regulate expression of are the cyclins and the cyclin-dependent kinases that drive progression through the cell cycle. C-myc was found to bind the E-box of cyclins D1 and D2, CDK4, and cyclin B1 (Dang et al., 2006). CDK4 and both Cyclin D1 and D2 seem to be required for the c-myc transformation to cancer …show more content…
Since c-myc leads to increases in cell proliferation, it follows that the cell would require more protein to be able to function and to produce new daughter cells. C-myc has been shown to regulate genes that encode ribosomal RNAs and proteins that help to synthesize and piece together the ribosomes that function in protein synthesis (van Riggelen et al., 2010). Among these proteins are RNA polymerases I and III, which function in forming the substrate for these ribosomes, mRNA. While the overexpression of c-myc probably leads to a large cell size, it has not been determined if the ribosome biogenesis can lead to the development of neoplastic tissues (Dang et al., 2006).
Another functional group of genes that c-myc regulates the expression of are those that produce cytoskeletal and cell adhesion proteins. The first of these genes to be recognized were those encoding collagen. C-myc consistently repressed these genes across repeated experiments (Dang et al., 2006). N-cadherin is a protein involved in the regulation of hematopoietic stem cells and their movement from the bone marrow out into tissues to mature. C-myc has been found to repress transcription of this gene