Proto-Oncogenes and Oncogenes - Essay Example

Proto-Oncogenes and Oncogenes PROTO-ONCOGENES AND ONCOGENES Out of the approximately 35,000 genes present in the genome of humans, only a small number are related to cancer. Alterations present in the same gene are normally associated with various cancer types, and these malfunctioning genes are classified into proto-oncogenes, tumor suppressors, and DNA repair genes (Hanahan & Weinberg 2011, p. 650). Proto-oncogenes code for and produce protein products for the inhibition of normal apoptosis or enhancement of cell division, while tumor suppressors produce proteins meant to cause cell death or prevent cell division.

Tumor suppressors and proto-oncogenes act in the same way as the brakes and accelerator in a vehicle respectively. Controlled growth of cells is maintained through the regulative activity of tumor suppressors that slow the growth of cells and proto-oncogenes that accelerate cell growth (Hanahan & Weinberg 2011, p. 650). Uncontrolled cell growth will occur when proto-oncogenes mutate to form oncogenes and accelerate the growth of cells or if tumor suppressors mutate to prevent growth inhibition. Proto-oncogenes in normal cells are responsible for the production of proteins that stimulate the division of the cell through signals to the nucleus.

The proteins involved in this signaling process, act through the signal transduction pathway or cascade that is made up of a series of steps (Bock & Marsh 2010, p. 32). The pathway is inclusive of a membrane receptor that binds the signal molecule, cytoplasmic proteins that convey the signal, and transcription factors that activate the cell division-related genes in the nucleus. Each of the cascade’s steps has a protein or factor that activates another, although some of these factors have the ability to activate more than one cellular protein.

Oncogenes, on the other hand, are altered proto-oncogenes that are involved in coding for the molecules in signaling. They continuously activate the signaling pathway, which results in heightened factor or protein production, especially those involved in the stimulation of growth (Schwab 2013, p. 21). For example, the MYC proto-oncogene codes for transcription factors and is converted to an oncogene that is related to over two-thirds of all cancers. Ras, on the other hand, is an oncogene that acts as a switch in the pathways and mutations cause the pathway to remain in the on mode and cause uncontrolled growth of cells.

In order for a proto-oncogene to be converted to an oncogene, its original function is modified through any of three basic activation methods. The first activation method involves a mutation in the proto-oncogene (Weinberg 2013, p. 115), as well as within a region involved in regulation, such as the promoter region, resulting in alterations in the structure of the proteins. This could result in either loss of regulatory ability or an increase in the activity of an enzyme or protein. Another activation method is an increase in particular protein concentration that is caused by gene duplication that results in increased cellular protein levels.

In addition, this can also be caused by an increase in the stability of protein messenger RNA, which prolongs its activity through increasing its existence, as well as misregulation which increases the expression of proteins. Finally, activation also occurs through chromosomal translocation which can be contemplated as an abnormality of the chromosome (Weinberg 2013, p. 122). For example, translocation events that lead to the relocation of proto-oncogenes to new sites on the chromosome could result in increased expression.

In addition, translocation events that cause fusion between proto-oncogenes and another gene could also lead to the activation of proto-oncogenes, creating a protein of fusion with heightened oncogenic activity.