Missense Mutant p53 Transactivates Wnt/β-Catenin Signaling in Neighboring p53-Destabilized Cells through the COX-2/PGE2 Pathway

Cancer Res Commun. 2025 Jan 1;5(1):13-23. doi: 10.1158/2767-9764.CRC-24-0471.

Abstract

There is intratumor heterogeneity in the stabilization of missense mutant p53, and it has been thought that only cells with nuclear accumulation of mutant p53 have oncogenic function. However, using mouse intestinal tumor-derived organoids, we show that mutant p53-stabilized cells transactivate Wnt/β-catenin signaling in neighboring p53-destabilized cells through activating the COX-2/PGE2 pathway. These results suggest that both p53-stabilized cells and p53-destabilized cells contribute to malignant progression through interaction within the intratumor microenvironment.

MeSH terms

  • Animals
  • Cyclooxygenase 2* / genetics
  • Cyclooxygenase 2* / metabolism
  • Dinoprostone* / metabolism
  • Humans
  • Mice
  • Mutation, Missense*
  • Organoids / metabolism
  • Organoids / pathology
  • Tumor Microenvironment
  • Tumor Suppressor Protein p53* / genetics
  • Tumor Suppressor Protein p53* / metabolism
  • Wnt Signaling Pathway* / genetics
  • beta Catenin / genetics
  • beta Catenin / metabolism

Substances

  • Tumor Suppressor Protein p53
  • Cyclooxygenase 2
  • Dinoprostone
  • beta Catenin
  • TP53 protein, human
  • Trp53 protein, mouse