Regulation of Cancer Stem Cells: Lysine Methylation of p53

The highly studied p53 protein regulates multiple transitions through the cell cycle effectively halting the growth of tumorlike masses.[1] This gene was primitively identified an oncogene; however, it was later derived that p53 functions as a tumor suppressor.[1] Named due to its mass in kDa, p53 is a phosphoprotein comprised of 393 amino acids.[1] Normal cells contain controlled, small quantities of p53 in order to facilitate the regulation of normal cell activities such as growth arrest, senescence,DNArepair, and apoptosis.[1,2] These features are pivotal the continuation of healthy cell production. Constructively, the functions of p53 work together to pause the cell growth cycles in order to address and repair certain sequences of DNA if needed before cell division commences. If repair cannot be completed, then p53 signals for the cell to become senescent and/or later to destroy itself via apoptosis.[1] Upon DNA damage and other cellular stressors, the quantity of p53 is upregulated in order to instigate either the repair or apoptotic cellular pathways; however, continued high levels of p53 are detrimental as its increased ability to activate the apoptotic pathway is likened to an accelerated aging process.[1] The C-terminus domain (CTD) of p53 contains several modifiable lysine residues that may be augmented in different patterns resulting in an array of dissimilar protein-protein interactions thus greatly adding to the multiplicity of functions for the protein itself. This study aims to show that the control of these modifications may not only reduce the causation of multiple forms of cancers but may also be used as a preventative mechanism by never allowing malignant masses to have formed in the firstplace