A new study examined the relationship between the gain-of-function of the p53 protein in cells and the impact of aneuploidy. There is a goal to develop a medication that can restore p53’s normal role to reduce cancer.
Experts at Vanderbilt University Medical Center recently published research that demonstrates how aneuploidy controls phenotypes in p53 mutant cells. The findings suggest that the medications available for a specific gain-of-function mutant cell should alter in composition, and their impact on chromosome changes should be evaluated. Lindsay Redman-Rivera, a biochemistry expert at the institution, and Jennifer Pietenpol, director of the Vanderbilt-Ingram Cancer Center, led the study.
Exploring what p53 exactly is
p53 is a tumor suppressor protein that has been found to be mutated in more than half of all human malignancies according to the National Cancer Institute. Recently, it was discovered that the mutant protein cell p53 had acquired a new ability called gain-of-function, which might lead to novel carcinogenic phenotypes due to its own high The first investigations on the p53 protein demonstrate that mutant cells lose their suppressive function, which is responsible for removing wild-type tumors.
Drugs that restore the functions of the p53 protein have recently been identified by the expert as reported by NewsMedical, 400 clinical trials will be conducted on the selected drugs to determine which drug is most effective at restoring the natural cancer-killing function of the cell.
The mutant p53 has been studied over the past three decades after it was discovered to have an abnormality. According to the authors, there has been a long debate in the oncology community over whether there are difficulties when mutant protein cell overexpression reaches a peak and leads to the emergence of oncogenic characteristics.
The correlation between p53 and aneuploidy
Numerous studies have been conducted in an attempt to understand the protein p53’s inherent ability, but the results have been mixed. As explained in Nature Communications, because of its own high-frequency expressions, the mutant p53 gain-of-function was thought to exist. If it continues to lose its suppressive capacity and is produced excessively, p53 mutants, like other normal genes, can contribute to tumor growth and may result in severe cancer situations. Meanwhile, investigations focusing on approaches for reviving the functioning of native genes such as p53 are lacking in data. However, a recent study may hold the key to resolving the speeding up of cancer cell aggressive phenotypes.
The new study added to prior research on the link between the p53 mutation and aneuploidy, or the aberrant increase or loss of chromosomes. This genetic condition has the potential to disrupt not only the ability of p53 cells, but also the growth of malignant cells and carcinogenesis.
The p53 cells were examined using CRISPR-Cas9 technology. Experts were able to create two identical cell lines with p53 mutations using the gene-editing technology. The in vitro gain-of-function phenotypic cell lines had increased aneuploidy, according to the findings.
The gain-of-function was shown to be unaffected by p53 mutations. Furthermore, whether or not the p53 mutation is present, the high rate of aneuploidy in malignancies has resulted in a poor prognosis.