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Though smoking leads to an overall decrease in DNA methylation, several critical genes become hypermethylated. Two of the most noteworthy of these genes are p16 and p53. These genes are critical to cell cycle regulation and were shown to have higher levels of methylation in smokers than in non smokers. [3]
p53, also known as Tumor protein P53, cellular tumor antigen p53 (UniProt name), or transformation-related protein 53 (TRP53) is a regulatory protein that is often mutated in human cancers. The p53 proteins (originally thought to be, and often spoken of as, a single protein) are crucial in vertebrates, where they prevent cancer formation. [5]
The p53 p63 p73 family is a family of tumor suppressor genes. [1] [2] This gene family codes the proteins: p53; TP73L (also known as "p63") p73; They are sometimes considered part of a "p53 family." When overexpressed, these proteins are known to be involved in tumor pathogenesis. [3]
The p53 protein was discovered 10 years earlier by several groups, including that of David Lane and Lionel Crawford, Arnold Levine, and Lloyd Old. But there was no evidence that p53 played a major role in human cancers, and the gene encoding p53 (TP53) was thought to be an oncogene rather than a tumor suppressor gene.
P53, a transcription factor, can bind two sites within the human TIGAR gene to activate expression. [9] [13] One site is found within the first intron, and binds p53 with high affinity. [9] [13] The second is found just prior to the first exon, binds p53 with low affinity, [9] [13] and is conserved between mice and humans. [9]
This gene is a transcription factor that regulates the cell cycle and hence functions as a tumor suppressor. By inducing G ( guanine ) to T ( thymidine ) transversions in transversion hotspots within p53 , there is a probability that benzo[ a ]pyrene diol epoxide inactivates the tumor suppression ability in certain cells, leading to cancer.
WRAP53 (also known as WD40-encoding RNA antisense to p53) is a gene implicated in cancer development. The name was coined in 2009 to describe the dual role of this gene, encoding both an antisense RNA that regulates the p53 tumor suppressor and a protein involved in DNA repair, telomere elongation and maintenance of nuclear organelles Cajal bodies (Figure 1).
The previous finding of RTVP1 (GLIPR1) as a p53 target gene with tumor suppressor functions prompted the researches to initiate a genome-wide sequence homology search for RTVP1/GLIPR1-like (GLIPR1L) genes. [8] p53, the tumor suppressor gene is the most commonly mutated gene in human cancer. [8] Mutation in p53 gene can lead to cellular ...