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Deciphering the Role of p53 and TAp73 in Neuroblastoma: From Pathogenesis to Treatment

Joana Almeida1, Inês Mota1, Jan Skoda2,3

  • 1LAQV/REQUIMTE, Laboratory of Microbiology, Department of Biological Sciences, Faculty of Pharmacy, University of Porto, Rua de Jorge Viterbo Ferreira 228, 4050-313 Porto, Portugal.

Cancers
|December 23, 2022
PubMed

Insights

Neuroblastoma, a common childhood cancer, involves the p53/TAp73 pathway. Inhibited p53/TAp73 activity and its interplay with N-MYC and microRNAs are key in neuroblastoma development and drug resistance.

Area of Science:

  • Pediatric Oncology
  • Cancer Biology
  • Molecular Oncology

Background:

  • Neuroblastoma (NB) is a prevalent pediatric cancer originating from neural crest stem cells.
  • Its clinical variability presents significant therapeutic challenges in pediatric oncology.
  • The p53 family proteins, p53 and TAp73, are crucial in preventing genomic instability and malignant transformation.

Purpose of the Study:

  • To review the critical role of the p53/TAp73 pathway in neuroblastoma pathogenesis.
  • To highlight potential therapeutic strategies targeting this pathway.
  • To explore the interplay between p53/TAp73, N-MYC, and microRNAs in NB.

Main Methods:

  • Literature review focusing on the p53/TAp73 pathway in neuroblastoma.
  • Analysis of interactions with inhibitory proteins (MDM2, MDMX, mutant p53, ΔNp73, Itch, Aurora kinase A).
  • Examination of the crosstalk between p53/TAp73, N-MYC, and microRNAs.

Main Results:

  • p53/TAp73 activities are frequently inhibited in NB by various proteins.
  • N-MYC, a poor prognosis biomarker, significantly influences NB pathogenesis through interplay with p53/TAp73.
  • MicroRNAs show a significant crosstalk with p53/TAp73, offering therapeutic potential.

Conclusions:

  • The p53/TAp73 pathway is central to neuroblastoma pathogenesis.
  • Targeting the p53/TAp73 pathway, its regulators, and interacting molecules like N-MYC and miRNAs offers promising therapeutic avenues for NB.
  • Understanding these molecular interactions is vital for advancing alternative neuroblastoma treatments.
Keywords:
N-MYCmiRNAsneuroblastomap53 family proteinstargeted anticancer therapy

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