Free Essay on the Role and Functions of P53 in Tumor

Background Information on p53

P53 also known as the tumor protein or TP53 is a gene in the human body coding for protein regulating the cell cycle to function as the body tumor suppressor. The above protein is fundamental various cells especially in the multicellular types of organisms to acts as cancers suppressors. To some individuals, they describe p53 as the genome guardian referring to its role, as stability conserving be genome preventions. Its history dates in the year 1979 by Arnold Levine and William Old at Princeton University and Sloan memorial respectively(Chen,2016).However, the presence of this kind of suppressor existed much earlier as the major target for the SV40 virus, which was kind of, strains that induced tumors development. Human p53 type of gene is located mainly at the seventeenth types of chromosome also known as (17p13.1).The structure of p53 is majorly a phosphoprotein that consists of 395 amino acids alongside four major domains that include:

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A domain that activates transcription factors

The domain that recognizes such kind of DNA sequence

Protein Tetramerization Domain

The domain that helps in recognizing the damaged DNA such as the single-stranded domain

Mechanism

The p53 gene plays an important and a most fundamental role in the process of apoptosis as well as in the cell cycle control mechanism. Beside, defective p53 in most cases can help allow the abnormal cells in proliferation those results in cancer attacks (Chen, 2016).However, the normal cells in most cases have a low level of p53 protein level.

Just like most gene, most of the available p53 are commonly produced specific kinds of tumor suppressor TP35gene.

The most common brain tumor associated with p53 is the malignant glioma; the condition associated with the poor prognosis. Most of the common mutation in the p53 turmoil suppressor detection majorly occurs in the gliomas (Chen, 2016).Moreover, p53 plays a role in in the process of inducing cell cycle arrest senescence, apoptosis or even differentiation following various mechanisms in the cellular stress.

The p53 tumor suppressor is deleted in the human tumors and can easily lose during the process of glioma formation. Consequently, the gene p53 can trigger a different kind of cellular programs such as apoptosis, cycle arrests differentiation and the process of DNA repairs.

The link between P53 and the Apoptosis

The p53 suppressor acts to help integrate different kinds of multiple stress signals into a series of multiple and proliferative responses. One of the most critical importance of p53 is the ability positively activate positive apoptosis in which the disruption of the above process is likely to stimulate tumor progression as well as the chemoresistance (Chen, 2016). The major link between p53 and apoptosis is that it promotes the process of apoptosis majorly through transcription-independent and independent mechanisms a process that ensures any form of cell death programs proceeds more smoothly as intended.

Moreover, the apoptotic activity in line with p53 is controlled through integrated series of quantitative and qualitative events that in most cases positively or negatively influence the possible outcomes of p53activational procedures.

More importantly, the tumor suppressor acts to reduce or to maintain the process of tissues homeostatic aimed at controlling different cells behaviors within a particular cell tissue in the given organisms. To achieve such a mechanism, cells typically different kinds of process to prevent any form of aberrant cells proliferation. Besides, p53 can easily be activated by hypoxia, or the DNA damages to promote different kinds of cell-cycle diverse checkpoints cellular senescence, DNA repairs and the process of apoptosis.Following different and diverse proliferative advantages that are produced by the sudden loss of p53, it is clear that p53 is the major cause of the brain tumor gene in human cancer (England, Huang, & Karsy, 2013). Consequently, the p53 was identified as the major suppressor of the genome, based on their ability to precisely meditate G1 arrest following incidents that occur on DNA damages of whichever the part of the brain.

The link between P53 and Brain Tumor

The p53 tumor gene also known as the suppressor gene is one of the most and frequently altered human gene in human cancer. Besides, it s the kind of gene found mutated in several forms among the possible human genes. Loss of p53 within the human body plays a vital role regarding cancer development (England, Huang, & Karsy, 2013). The major foundation by which p53 alters and triggers tumorigeneses are characterized but biochemical pathways towards designing a better performed biochemical pathways. Some of the recent investigations on the intracellular pathways mechanisms especially at the origin of p53 suppressive functions critically show that p53 is a major transcription factor towards detecting some of the most common cellular insults towards inducing a cellular response, apoptosis the cell growth mechanisms.

Method and Experiment how to Test the impact of p53 on Glioma Growth

Experiment:

Assume your experiment on testing the possible impacts of p53 on the growth of Glioma and you are provided with 50% of glioblastomas cerebral glioma. Testing of the above hypothesis involves analyzing the expression of p53 on the glioma in a more decent laboratory matter with the use of modern technological advance (Bieging, Mello, & Attardi, 2014). In the experiment, our hypothesis outcome is based on the fact that, on the formation of lines would be a direct representation of the possible positive result of the ontogeny on the presence of glioblastoma and their expected general use would lead to a more precise report.

Required material and the Expected experiment

In the experiment, the expression and the identification of p53 on glioma growth are determined using the blotting experiments following extraction from cytoplasmic RNA and from16 glioma cell lines.

Use of the glioma cell line, given that most of their cellular conditions as was discussed previously are known to be more reliable to give a more positive unbiased results. Besides, it is to derive all the cells to be used for globalization to avoid possible confusion

Use of RNA hybridization and isolation, just on the same effects, RNA is isolated from the solid tumor or even from the cells lines which are then used to perform a northern kind of blotting, following a random kind of labeled probes(Bieging, Mello, & Attardi, 2014). The other next step is the sequencing and the p53 amplification using the primers p53IN4ALand p53IN7BL major for the exon. The next step involves mixing of the available formed lines on the DNA especially of the three other independent available PCR reactants which are then mixed and amplified to give a strata gene Other steps would follow, transient, and the transfection bioassay, that involves introductions of the recipients p53 cells. On the end of the test is the determination of tumorigenicity in Nude Mice and finally on the Immunoprecipitation that involves washing of some of the common conflicting cells and labeling.

References

Bieging, K. T., Mello, S. S., &Attardi, L. D. (2014). Unravelling mechanisms of p53-mediated tumor suppression. Nature Reviews Cancer, 14(5), 359.

England, B., Huang, T., & Karsy, M. (2013). Current understanding of the role and targeting of tumor suppressor p53 in glioblastoma multiforme. Tumor Biology, 34(4), 2063-2074.

Chen, J. (2016). The Cell-Cycle Arrest and Apoptotic Functions of p53 in Tumor Initiation and Progression. Cold Spring Harbor perspectives in medicine, 6(3), a026104-a026104.