Cancer is defined as a diverse state in which cells multiply, proliferate and spread through surrounding tissues. With all the different types of cancers we have, at least one originates from closely every cell type in the human body (Vogeistein and Kinzier,1992). Different influence can affect the processes of the cell cycle in both positive and negative ways. Tumor suppressor gene p53 is among the negative regulators of the cell cycle if affected by alteration, mutations or by interaction with oncogene products of DNA tumor viruses. All these mutations cause genetic changes in the cells and lead to cancer (Levine , Finlay, and Momand, 1991). TP53 plays an important role in tumor prevention, and gene stability and this have been demonstrated
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The loss of its function initiates the formation of tumors, which has been shown in patients with Li-Fraumeni Syndrome (Feng et al, 2017). About 50% of these patients develop different kinds of cancers like breast cancer, sarcoma, and brain cancer at age 30 (Bennett et al, 1994). Three processes involves the activation of p53 in response to stress signal; sequence-specific DNA binding, stabilization of p53, and transcriptional activation of target gene (Lowe and Zilfou. 2009). Circumstances like a negative regulator that mediates ubiquitin-mediated degradation of p53 can impede p53 interaction with Mdm2 which causes p53 stabilization. For instance, when events like chemotherapeutic agent or ionizing radiation causes damage to DNA, p53 is post translationally modified. Different kinases like ATM, ATR, DNA-PK, Chk1, and Chk2 phosphorylate the amino terminus of p53 at specific amino acids and this prevent the binding of Mdm2 (Minute double minute 2). Also an oncogenic challenge to the cell through antagonism of the p53-Mdm2 interaction by the tumor suppressor p14ARF helps in p53 stabilization (Lowe and Zilfou. 2009, Nakagawara et al. 2011, and Nakamura et
The loss of its function initiates the formation of tumors, which has been shown in patients with Li-Fraumeni Syndrome (Feng et al, 2017). About 50% of these patients develop different kinds of cancers like breast cancer, sarcoma, and brain cancer at age 30 (Bennett et al, 1994). Three processes involves the activation of p53 in response to stress signal; sequence-specific DNA binding, stabilization of p53, and transcriptional activation of target gene (Lowe and Zilfou. 2009). Circumstances like a negative regulator that mediates ubiquitin-mediated degradation of p53 can impede p53 interaction with Mdm2 which causes p53 stabilization. For instance, when events like chemotherapeutic agent or ionizing radiation causes damage to DNA, p53 is post translationally modified. Different kinases like ATM, ATR, DNA-PK, Chk1, and Chk2 phosphorylate the amino terminus of p53 at specific amino acids and this prevent the binding of Mdm2 (Minute double minute 2). Also an oncogenic challenge to the cell through antagonism of the p53-Mdm2 interaction by the tumor suppressor p14ARF helps in p53 stabilization (Lowe and Zilfou. 2009, Nakagawara et al. 2011, and Nakamura et