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MDMX in Cancer: A Partner of p53 and a p53-Independent Effector
- Source :
- Biologics: Targets & Therapy, Vol Volume 18, Pp 61-78 (2024)
- Publication Year :
- 2024
- Publisher :
- Dove Medical Press, 2024.
-
Abstract
- Wu Lin,1,* Yuxiang Yan,2,* Qingling Huang,1 Dali Zheng2 1Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Fujian Medical University, Fuzhou, People’s Republic of China; 2Fujian Key Laboratory of Oral Diseases, School and Hospital of Stomatology, Fujian Medical University, Fuzhou, People’s Republic of China*These authors contributed equally to this workCorrespondence: Dali Zheng, Fujian Key Laboratory of Oral Diseases, School and Hospital of Stomatology, Fujian Medical University, 88 Jiao Tong Road, Fuzhou, 350004, People’s Republic of China, Email dalizheng@fjmu.edu.cnAbstract: The p53 tumor suppressor protein plays an important role in physiological and pathological processes. MDM2 and its homolog MDMX are the most important negative regulators of p53. Many studies have shown that MDMX promotes the growth of cancer cells by influencing the regulation of the downstream target gene of tumor suppressor p53. Studies have found that inhibiting the MDMX-p53 interaction can effectively restore the tumor suppressor activity of p53. MDMX has growth-promoting activities without p53 or in the presence of mutant p53. Therefore, it is extremely important to study the function of MDMX in tumorigenesis, progression and prognosis. This article mainly reviews the current research progress and mechanism on MDMX function, summarizes known MDMX inhibitors and provides new ideas for the development of more specific and effective MDMX inhibitors for cancer treatment.Keywords: MDMX, P53, cancer, inhibitors
- Subjects :
- mdmx
p53
cancer
inhibitors
Medicine (General)
R5-920
Subjects
Details
- Language :
- English
- ISSN :
- 11775491
- Volume :
- ume 18
- Database :
- Directory of Open Access Journals
- Journal :
- Biologics: Targets & Therapy
- Publication Type :
- Academic Journal
- Accession number :
- edsdoj.0fa4579a796e4fed85d17b0f12d9f956
- Document Type :
- article