Cellular responses to mutagenic injury
Mutagens have the potential to cause DNA damage; however, most cells that acquire DNA damage do not pose a risk for cancer development in the host organism. One main reason why DNA damage does not always translate into tumor formation is that only 1.5% of the entire genome is responsible for coding proteins.
As such, DNA mutations occurring in the remaining 98.5% of the genome will not directly lead to dysregulated protein synthesis. However, it is well recognized that non-coding DNA plays a critical role in gene expression through various mechanisms, including long non-coding RNA and microRNA (Lange et al., 2021). In the event a mutation does occur in an exome region, control of the cell cycle is central to safeguarding against cancer development, and cells that acquire DNA alterations can induce cell cycle arrest, programmed cell death, or both. Dysregulation within these two key cellular programs (i.e., cell cycle arrest and apoptosis) predisposes to genomic instability and a consequent increased risk for tumor formation.
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