Targeting the p53-MDM2 pathway for neuroblastoma therapy: Rays of hope
Despite being the subject of extensive research and clinical trials, neuroblastoma remains a major therapeutic challenge in pediatric oncology. The p53 protein is a central safeguard that protects cells against genome instability and malignant transformation. Mutated TP53 (the gene encoding p53) is...
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| Published in | Cancer letters Vol. 496; pp. 16 - 29 |
|---|---|
| Main Authors | , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Ireland
Elsevier B.V
01.01.2021
Elsevier Limited |
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| Online Access | Get full text |
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| Abstract | Despite being the subject of extensive research and clinical trials, neuroblastoma remains a major therapeutic challenge in pediatric oncology. The p53 protein is a central safeguard that protects cells against genome instability and malignant transformation. Mutated TP53 (the gene encoding p53) is implicated in many human cancers, but the majority of neuroblastomas have wild type p53 with intact transcriptional function. In fact, the TP53 mutation rate does not exceed 1–2% in neuroblastomas. However, overexpression of the murine double minute 2 (MDM2) gene in neuroblastoma is relatively common, and leads to inhibition of p53. It is also associated with other non-canonical p53-independent functions, including drug resistance and increased translation of MYCN and VEGF mRNA. The p53-MDM2 pathway in neuroblastoma is also modulated at several different molecular levels, including via interactions with other proteins (MYCN, p14ARF). In addition, the overexpression of MDM2 in tumors is linked to a poorer prognosis for cancer patients. Thus, restoring p53 function by inhibiting its interaction with MDM2 is a potential therapeutic strategy for neuroblastoma. A number of p53-MDM2 antagonists have been designed and studied for this purpose. This review summarizes the current understanding of p53 biology and the p53-dependent and -independent oncogenic functions of MDM2 in neuroblastoma, and also the regulation of the p53-MDM2 axis in neuroblastoma. This review also highlights the use of MDM2 as a molecular target for the disease, and describes the MDM2 inhibitors currently being investigated in preclinical and clinical studies. We also briefly explain the various strategies that have been used and future directions to take in the development of effective MDM2 inhibitors for neuroblastoma.
•Targeting p53-MDM2 Pathway is a validated approach for neuroblastoma Therapy.•MDM2 overexpression and constitutive activation are common in neuroblastoma.•MDM2 promotes chemical-induced carcinogenesis.•MDM2 promotes cancer progression by regulating multiple cellular functions; and.•MDM2 inhibitors have anticancer activity in neuroblastoma models. |
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| AbstractList | Despite being the subject of extensive research and clinical trials, neuroblastoma remains a major therapeutic challenge in pediatric oncology. The p53 protein is a central safeguard that protects cells against genome instability and malignant transformation. Mutated TP53 (the gene encoding p53) is implicated in many human cancers, but the majority of neuroblastomas have wild type p53 with intact transcriptional function. In fact, the TP53 mutation rate does not exceed 1–2% in neuroblastomas. However, overexpression of the murine double minute 2 (MDM2) gene in neuroblastoma is relatively common, and leads to inhibition of p53. It is also associated with other non-canonical p53-independent functions, including drug resistance and increased translation of MYCN and VEGF mRNA. The p53-MDM2 pathway in neuroblastoma is also modulated at several different molecular levels, including via interactions with other proteins (MYCN, p14ARF). In addition, the overexpression of MDM2 in tumors is linked to a poorer prognosis for cancer patients. Thus, restoring p53 function by inhibiting its interaction with MDM2 is a potential therapeutic strategy for neuroblastoma. A number of p53-MDM2 antagonists have been designed and studied for this purpose. This review summarizes the current understanding of p53 biology and the p53-dependent and -independent oncogenic functions of MDM2 in neuroblastoma, and also the regulation of the p53-MDM2 axis in neuroblastoma. This review also highlights the use of MDM2 as a molecular target for the disease, and describes the MDM2 inhibitors currently being investigated in preclinical and clinical studies. We also briefly explain the various strategies that have been used and future directions to take in the development of effective MDM2 inhibitors for neuroblastoma. Despite being the subject of extensive research and clinical trials, neuroblastoma remains a major therapeutic challenge in pediatric oncology. The p53 protein is a central safeguard that protects cells against genome instability and malignant transformation. Mutated TP53 (the gene encoding p53) is implicated in many human cancers, but the majority of neuroblastomas have wild type p53 with intact transcriptional function. In fact, the TP53 mutation rate does not exceed 1-2% in neuroblastomas. However, overexpression of the murine double minute 2 (MDM2) gene in neuroblastoma is relatively common, and leads to inhibition of p53. It is also associated with other non-canonical p53-independent functions, including drug resistance and increased translation of MYCN and VEGF mRNA. The p53-MDM2 pathway in neuroblastoma is also modulated at several different molecular levels, including via interactions with other proteins (MYCN, p14 ). In addition, the overexpression of MDM2 in tumors is linked to a poorer prognosis for cancer patients. Thus, restoring p53 function by inhibiting its interaction with MDM2 is a potential therapeutic strategy for neuroblastoma. A number of p53-MDM2 antagonists have been designed and studied for this purpose. This review summarizes the current understanding of p53 biology and the p53-dependent and -independent oncogenic functions of MDM2 in neuroblastoma, and also the regulation of the p53-MDM2 axis in neuroblastoma. This review also highlights the use of MDM2 as a molecular target for the disease, and describes the MDM2 inhibitors currently being investigated in preclinical and clinical studies. We also briefly explain the various strategies that have been used and future directions to take in the development of effective MDM2 inhibitors for neuroblastoma. Despite being the subject of extensive research and clinical trials, neuroblastoma remains a major therapeutic challenge in pediatric oncology. The p53 protein is a central safeguard that protects cells against genome instability and malignant transformation. Mutated TP53 (the gene encoding p53) is implicated in many human cancers, but the majority of neuroblastomas have wild type p53 with intact transcriptional function. In fact, the TP53 mutation rate does not exceed 1-2% in neuroblastomas. However, overexpression of the murine double minute 2 (MDM2) gene in neuroblastoma is relatively common, and leads to inhibition of p53. It is also associated with other non-canonical p53-independent functions, including drug resistance and increased translation of MYCN and VEGF mRNA. The p53-MDM2 pathway in neuroblastoma is also modulated at several different molecular levels, including via interactions with other proteins (MYCN, p14ARF). In addition, the overexpression of MDM2 in tumors is linked to a poorer prognosis for cancer patients. Thus, restoring p53 function by inhibiting its interaction with MDM2 is a potential therapeutic strategy for neuroblastoma. A number of p53-MDM2 antagonists have been designed and studied for this purpose. This review summarizes the current understanding of p53 biology and the p53-dependent and -independent oncogenic functions of MDM2 in neuroblastoma, and also the regulation of the p53-MDM2 axis in neuroblastoma. This review also highlights the use of MDM2 as a molecular target for the disease, and describes the MDM2 inhibitors currently being investigated in preclinical and clinical studies. We also briefly explain the various strategies that have been used and future directions to take in the development of effective MDM2 inhibitors for neuroblastoma.Despite being the subject of extensive research and clinical trials, neuroblastoma remains a major therapeutic challenge in pediatric oncology. The p53 protein is a central safeguard that protects cells against genome instability and malignant transformation. Mutated TP53 (the gene encoding p53) is implicated in many human cancers, but the majority of neuroblastomas have wild type p53 with intact transcriptional function. In fact, the TP53 mutation rate does not exceed 1-2% in neuroblastomas. However, overexpression of the murine double minute 2 (MDM2) gene in neuroblastoma is relatively common, and leads to inhibition of p53. It is also associated with other non-canonical p53-independent functions, including drug resistance and increased translation of MYCN and VEGF mRNA. The p53-MDM2 pathway in neuroblastoma is also modulated at several different molecular levels, including via interactions with other proteins (MYCN, p14ARF). In addition, the overexpression of MDM2 in tumors is linked to a poorer prognosis for cancer patients. Thus, restoring p53 function by inhibiting its interaction with MDM2 is a potential therapeutic strategy for neuroblastoma. A number of p53-MDM2 antagonists have been designed and studied for this purpose. This review summarizes the current understanding of p53 biology and the p53-dependent and -independent oncogenic functions of MDM2 in neuroblastoma, and also the regulation of the p53-MDM2 axis in neuroblastoma. This review also highlights the use of MDM2 as a molecular target for the disease, and describes the MDM2 inhibitors currently being investigated in preclinical and clinical studies. We also briefly explain the various strategies that have been used and future directions to take in the development of effective MDM2 inhibitors for neuroblastoma. Despite being the subject of extensive research and clinical trials, neuroblastoma remains a major therapeutic challenge in pediatric oncology. The p53 protein is a central safeguard that protects cells against genome instability and malignant transformation. Mutated TP53 (the gene encoding p53) is implicated in many human cancers, but the majority of neuroblastomas have wild type p53 with intact transcriptional function. In fact, the TP53 mutation rate does not exceed 1–2% in neuroblastomas. However, overexpression of the murine double minute 2 (MDM2) gene in neuroblastoma is relatively common, and leads to inhibition of p53. It is also associated with other non-canonical p53-independent functions, including drug resistance and increased translation of MYCN and VEGF mRNA. The p53-MDM2 pathway in neuroblastoma is also modulated at several different molecular levels, including via interactions with other proteins (MYCN, p14ARF). In addition, the overexpression of MDM2 in tumors is linked to a poorer prognosis for cancer patients. Thus, restoring p53 function by inhibiting its interaction with MDM2 is a potential therapeutic strategy for neuroblastoma. A number of p53-MDM2 antagonists have been designed and studied for this purpose. This review summarizes the current understanding of p53 biology and the p53-dependent and -independent oncogenic functions of MDM2 in neuroblastoma, and also the regulation of the p53-MDM2 axis in neuroblastoma. This review also highlights the use of MDM2 as a molecular target for the disease, and describes the MDM2 inhibitors currently being investigated in preclinical and clinical studies. We also briefly explain the various strategies that have been used and future directions to take in the development of effective MDM2 inhibitors for neuroblastoma. •Targeting p53-MDM2 Pathway is a validated approach for neuroblastoma Therapy.•MDM2 overexpression and constitutive activation are common in neuroblastoma.•MDM2 promotes chemical-induced carcinogenesis.•MDM2 promotes cancer progression by regulating multiple cellular functions; and.•MDM2 inhibitors have anticancer activity in neuroblastoma models. Despite being the subject of extensive research and clinical trials, neuroblastoma remains a major therapeutic challenge in pediatric oncology. The p53 protein is a central safeguard that protects cells against genome instability and malignant transformation. Mutated TP53 (the gene encoding p53) is implicated in many human cancers, but the majority of neuroblastomas have wild type p53 with intact transcriptional function. In fact, the TP53 mutation rate does not exceed 1–2% in neuroblastomas. However, overexpression of the murine double minute 2 (MDM2) gene in neuroblastoma is relatively common, and leads to inhibition of p53. It is also associated with other non-canonical p53-independent functions, including drug resistance and increased translation of MYCN and VEGF mRNA. The p53-MDM2 pathway in neuroblastoma is also modulated at several different molecular levels, including via interactions with other proteins (MYCN, p14 ARF ). In addition, the overexpression of MDM2 in tumors is linked to a poorer prognosis for cancer patients. Thus, restoring p53 function by inhibiting its interaction with MDM2 is a potential therapeutic strategy for neuroblastoma. A number of p53-MDM2 antagonists have been designed and studied for this purpose. This review summarizes the current understanding of p53 biology and the p53-dependent and -independent oncogenic functions of MDM2 in neuroblastoma, and also the regulation of the p53-MDM2 axis in neuroblastoma. This review also highlights the use of MDM2 as a molecular target for the disease, and describes the MDM2 inhibitors currently being investigated in preclinical and clinical studies. We also briefly explain the various strategies that have been used and future directions to take in the development of effective MDM2 inhibitors for neuroblastoma. |
| Author | Liu, Gang Xian, Wa Wang, Wei Zhou, Jia Zafar, Atif McKeon, Frank Zhang, Ruiwen |
| AuthorAffiliation | 3 Chemical Biology Program, Department of Pharmacology and Toxicology, University of Texas Medical Branch, Galveston, TX 77555, USA 1 Department of Pharmacological and Pharmaceutical Sciences, College of Pharmacy, University of Houston, Houston, Texas 77204, USA 2 Drug Discovery Institute, University of Houston, Houston, Texas 77204, USA 4 Department of Biology and Biochemistry, University of Houston, Houston, TX 77204, USA |
| AuthorAffiliation_xml | – name: 4 Department of Biology and Biochemistry, University of Houston, Houston, TX 77204, USA – name: 2 Drug Discovery Institute, University of Houston, Houston, Texas 77204, USA – name: 1 Department of Pharmacological and Pharmaceutical Sciences, College of Pharmacy, University of Houston, Houston, Texas 77204, USA – name: 3 Chemical Biology Program, Department of Pharmacology and Toxicology, University of Texas Medical Branch, Galveston, TX 77555, USA |
| Author_xml | – sequence: 1 givenname: Atif surname: Zafar fullname: Zafar, Atif organization: Department of Pharmacological and Pharmaceutical Sciences, College of Pharmacy, University of Houston, Houston, TX, 77204, USA – sequence: 2 givenname: Wei surname: Wang fullname: Wang, Wei organization: Department of Pharmacological and Pharmaceutical Sciences, College of Pharmacy, University of Houston, Houston, TX, 77204, USA – sequence: 3 givenname: Gang surname: Liu fullname: Liu, Gang organization: Chemical Biology Program, Department of Pharmacology and Toxicology, University of Texas Medical Branch, Galveston, TX, 77555, USA – sequence: 4 givenname: Wa surname: Xian fullname: Xian, Wa organization: Department of Biology and Biochemistry, University of Houston, Houston, TX, 77204, USA – sequence: 5 givenname: Frank surname: McKeon fullname: McKeon, Frank organization: Department of Biology and Biochemistry, University of Houston, Houston, TX, 77204, USA – sequence: 6 givenname: Jia surname: Zhou fullname: Zhou, Jia organization: Chemical Biology Program, Department of Pharmacology and Toxicology, University of Texas Medical Branch, Galveston, TX, 77555, USA – sequence: 7 givenname: Ruiwen surname: Zhang fullname: Zhang, Ruiwen email: rzhang27@central.uh.edu organization: Department of Pharmacological and Pharmaceutical Sciences, College of Pharmacy, University of Houston, Houston, TX, 77204, USA |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/33007410$$D View this record in MEDLINE/PubMed |
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| Keywords | MDM2 Inhibitors Neuroblastoma Targeted therapy p53 |
| Language | English |
| License | Copyright © 2020 Elsevier B.V. All rights reserved. |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 ObjectType-Review-3 content type line 23 These authors are co-first authors. Study concept and design: WW, JZ, FM, and RZ; drafting of the manuscript: AZ, WW, and RZ; revision of the manuscript: WW, GL, XW, FM, JZ, and RZ; administrative, technical, or material support: WW, RZ; study supervision: WW, RZ. All authors have read and agreed to the published version of the manuscript. Author Contributions |
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| PublicationTitle | Cancer letters |
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| PublicationYear | 2021 |
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| SubjectTerms | Animals Antineoplastic Agents - therapeutic use Apoptosis Biology Cancer therapies Cell cycle Clinical trials Deoxyribonucleic acid DNA DNA damage Drug resistance Gene amplification Gene Expression Regulation, Neoplastic - drug effects Genomes Genomic instability Humans Inhibitors MDM2 MDM2 protein Medical prognosis Molecular Targeted Therapy Mutation Mutation rates Neuroblastoma Neuroblastoma - drug therapy Neuroblastoma - metabolism Neuroblastoma - pathology Oncology p53 p53 Protein Proteins Proto-Oncogene Proteins c-mdm2 - antagonists & inhibitors Signal transduction Targeted therapy Transcription Tumor Suppressor Protein p53 - antagonists & inhibitors Tumors Vascular endothelial growth factor |
| Title | Targeting the p53-MDM2 pathway for neuroblastoma therapy: Rays of hope |
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