دورية أكاديمية

Therapeutics Targeting p53-MDM2 Interaction to Induce Cancer Cell Death.

التفاصيل البيبلوغرافية
العنوان: Therapeutics Targeting p53-MDM2 Interaction to Induce Cancer Cell Death.
المؤلفون: Koo, Nayeong, Sharma, Arun K., Narayan, Satya
المصدر: International Journal of Molecular Sciences; May2022, Vol. 23 Issue 9, p5005-5005, 21p
مصطلحات موضوعية: CANCER cells, CELL death, P53 antioncogene, CELL cycle, DNA repair, CELL physiology
مستخلص: Named as the guardian of the genome, p53 is a tumor suppressor that regulates cell function, often through many different mechanisms such as DNA repair, apoptosis, cell cycle arrest, senescence, metabolism, and autophagy. One of the genes that p53 activates is MDM2, which forms a negative feedback loop since MDM2 induces the degradation of p53. When p53 activity is inhibited, damaged cells do not undergo cell cycle arrest or apoptosis. As 50% of human cancers inactivate p53 by mutation, current research focuses on reactivating p53 by developing drugs that target the p53-MDM2 interaction, which includes the binding of MDM2 and phosphorylation of p53. The objective of this article is to provide a short list and description of p53-MDM2 antagonists that may be excellent candidates for inducing cancer cell death. Relevant articles were searched for and identified using online databases such as PubMed and ScienceDirect. Increasing p53 levels, by targeting the p53-MDM2 interaction, can help p53 play its role as a tumor suppressor and induce cancer cell death. Researchers have identified different compounds that can act as inhibitors, either by directly binding to MDM2 or by modifying p53 with phosphorylation. The results associated with the drugs demonstrate the importance of targeting such interactions to inhibit cancer cell growth, which indicates that the use of the compounds may improve cancer therapeutics. [ABSTRACT FROM AUTHOR]
Copyright of International Journal of Molecular Sciences is the property of MDPI and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
قاعدة البيانات: Complementary Index
الوصف
تدمد:16616596
DOI:10.3390/ijms23095005