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Darya Yanushko1,2,3,4, Beatriz German Falcon1,2,3,4,5, Rana El Bizri1,2,3,4,6

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p53 loss in prostate cancer cells promotes invasion and metastasis by increasing cell plasticity and communication with cancer-associated fibroblasts. This highlights new therapeutic targets for aggressive prostate cancer.

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Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Metastasis

Background:

  • Prostate cancer is a heterogeneous disease with variable outcomes.
  • Mutations in tumor suppressor genes PTEN and TP53 are linked to metastasis and poor prognosis.
  • TP53 loss-induced aggressiveness and metastasis mechanisms are not fully understood.

Purpose of the Study:

  • To investigate the role of Trp53 deficiency in Pten-null prostate cancer progression.
  • To elucidate the mechanisms underlying TP53 loss-induced cell plasticity and metastasis.
  • To identify potential therapeutic targets for aggressive prostate cancer.

Main Methods:

  • Genetically engineered mouse models of prostate cancer.
  • Single-cell transcriptomic and chromatin accessibility analyses.
  • Histological examinations, in vivo, and organoid-based experiments.

Main Results:

  • Trp53 deficiency in Pten-null prostate epithelial cells (PECs) enhances invasive adenocarcinoma and metastasis.
  • A distinct epithelial cell population with induced Jak/Stat3 signaling and mesenchymal features was identified.
  • This cell signature is prevalent in high-risk and metastatic prostate tumors.
  • PEC plasticity involves bi-directional communication with cancer-associated fibroblasts (CAFs).

Conclusions:

  • p53 loss drives protumorigenic crosstalk between PECs and CAFs, promoting prostate cancer progression.
  • Targeting this crosstalk represents a potential therapeutic strategy for aggressive prostate cancer.
  • Identified cell plasticity mechanisms and Jak/Stat3 signaling as potential vulnerabilities.