Cancer arises when your cells grow uncontrollably and refuse to die when they should die. Generally, your body is equipped with regulatory processes to prevent this chaos. Such a mechanism contains a protein called P53. Often dubbing the “mentor of genome”, this protein plays an important role in ensuring that your cells grow, divide and die in a systematic fashion. When P53 malfunction, results often occur cancer.
Learning about the works of P53 has not only deepened how scientists understand cancer, but also provide promising avenues for new remedies.
In my work as a cancer researcher, I study the underlying mechanism of how tumors develop and oppose treatment. Considering how cancer cells bypass safety measures like P53, scientists can find better ways to prevent them, which can lead to more effective treatment for patients.
How P53 works
Each cell contains DNA which instructs how it functions. Over time, this instruction manual can accumulate errors due to various factors such as harmful ultraviolet rays, smoking or even natural wear and exposure to tear.
This is where P53 comes. It acts like a vigilance proofarider, detects errors in DNA and decides how to handle them. If the damage is minor, the P53 instructs the cell to fix it. But if the damage is beyond repair, P53 triggers a process called apoptosis, or programmed cell death, ensuring that defective cell cancer does not change.
In more than half of all human cancer, the P53 is either missing or relaxed. This often occurs when an encoded genes for P53 are mutated or removed. Without a functioning P53, errors in DNA are uncontrolled, allowing damaged cells to multiply and make tumors.
P53 target the path
Given its important role in preventing cancer, P53 has become a major goal for the development of the drug.
Over the years, scientists have designed various strategies to target the P53 route, or regulate the network controls of molecules to regulate cell development, repair DNA damage and to trigger cell death. Instead of acting alone, P53 interacts with many molecular routes – some of which are still searching – who help determine the fate of a cell.
The approach to treatment is aimed at restoring or copying the function of P53 in cells where it is messed up. For example, scientists have developed small molecules that can tie mutant P53 and stabilize its faulty structure, restore DNA’s ability to tie DNA and regulate genes. Medications such as Prima-1 and Mira-1 essentially “rescue” P53, allow it to resume its role as a sales patron.
Even when the P53 is missing, scientists can still target controlled procedures for the treatment of cancer. For example, drugs can activate apoptosis or health cell division in ways that mimic the normal function of P53. Medications such as ABT-737 or Navitoclax can block protein on the P53 route that usually prevent apoptosis, which can lead to cell death even when cell death is absent.
Targets P53 Overseer
Researchers are also investigating other proteins that interact with P53 as possible treatment options. Because the P53 route is highly complex, targeting different parts of this network presents both opportunities and challenges.
My colleagues and I am not required when it is not required when I have studied two other close related proteins that mark P53 for destruction. These protein, called MDM2 and MDMX, become very active in cancer and breaks P53.
Researchers have developed medicines to block MDM2 or MDMX, but it is often not enough to target just one of these proteins. If one is blocked, the other can step inside and continue to destroy the P53. Most existing drugs are also much better in blocking MDM2 than MDMX, which is due to subtle differences in later size, including a small area for P53. This makes MDM2 difficult for drugs designed to tie MDM2 effectively or reach MDMX.
To find molecules that bind both MDM2 and MDMX, researchers traditionally synthesize and test each molecule, which is often time-and-temperature. Conversely, my colleagues and I used computer modeling tools to simulate how thousands of molecules can interact with proteins, allowing us to reduce potential candidates more quickly.
We identified a small molecule that we called CPO that shows its promise in its ability to target both MDM2 and MDMX. Our model has shown that CPO may have a strong ability to block both MDM2 and MDMX compared to another molecule that researchers earlier found that both these proteins could disrupt the cell culture.
More research is required to confirm whether the CPO works in living systems, similarly it does in the predictions of our computer. If the CPO is safe and effective in cells and animal models, it can provide another treatment option for cancer where MDM2 and MDMX are very active.
P53 and Cancer Treatment
The journey to fully exploit the P53 route for cancer medical science continues, and researchers are searching for many promising options.
Gon-editing technologies such as CRISPR are opening doors to correct P53 mutation directly into cancer cells.
Additionally, researchers are discovering combination treatments, which combine P53-targeting drugs with other treatments such as immunotherapy to increase their effectiveness.
Like other cancer remedies, a major challenge is to target P53 in drugs cancer cells and release healthy cells from unnecessary damage. Getting this balance would be important to translate these treatments from the lab to the clinic.
This article has been reinforced from the interaction, a non -profit, independent news organization, which brings you facts and reliable analysis to help you understand our complex world. It was written by: Prosper Obed Chukkeveka, University of pittxburg
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Prosper Obed Chukuvemeka does not work for funding from any company or organization, or benefits from this article, and will benefit from this article, and there is no relevant affiliation beyond their educational appointment.
