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Intestinal Apc-inactivation induces HSP25 dependency.

Sanne M van Neerven1,2,3,4, Wouter L Smit3,5, Milou S van Driel1,2,3,4

  • 1Laboratory for Experimental Oncology and Radiobiology, Center for Experimental and Molecular Medicine, Amsterdam UMC Location University of Amsterdam, Amsterdam, The Netherlands.

EMBO Molecular Medicine
|November 2, 2022
PubMed
Summary

Small heat shock protein 25 (HSP25) is crucial for colorectal cancer (CRC) initiation. Inhibiting HSP25 with brivudine reduced tumor development, offering a potential new prevention strategy.

Keywords:
Apc mutationsWnt signalingcolorectal cancerheat shock proteinsintestinal stem cells

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Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Colorectal cancers (CRCs) frequently arise from mutations in the APC tumor suppressor gene.
  • APC mutations activate the Wnt pathway, promoting cell proliferation and increasing protein synthesis demands.
  • Cancer cells rely on protein chaperones for proteostasis, but their role in CRC is not well understood.

Purpose of the Study:

  • To investigate the role of molecular chaperones in the initiation of colorectal cancer.
  • To identify specific chaperones involved in APC-driven intestinal transformation.

Main Methods:

  • Transcriptomic profiling of wild type and Apc-mutant murine organoids during transformation.
  • In vitro organoid cultures and mouse models to assess the function of small heat shock protein 25 (HSP25).
  • Chemical inhibition of HSP25 using brivudine to evaluate its effect on adenoma development.

Main Results:

  • A significant upregulation of Hspb1, encoding HSP25, was observed in Apc-mutant organoids.
  • HSP25 was found to be essential for APC-driven intestinal transformation in both organoid and mouse models.
  • Brivudine treatment, inhibiting HSP25, effectively reduced the development of premalignant adenomas.

Conclusions:

  • HSP25 plays a critical, previously unrecognized role in driving colorectal cancer initiation.
  • Targeting HSP25 represents a potential novel therapeutic vulnerability for CRC chemoprevention.
  • Inhibition of HSP25 may offer a strategy to prevent adenoma formation in high-risk individuals.