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Related Experiment Video

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Expression of R-Spondin 1 in ApcMin/+ Mice Suppresses Growth of Intestinal Adenomas by Altering Wnt and Transforming

Marianne Lähde1, Sarika Heino1, Jenny Högström2

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Gastroenterology
|September 17, 2020
PubMed
Summary

Overexpressing R-spondin 1 (RSPO1) in mice with intestinal tumors reduced tumor growth and increased survival. RSPO1 also inhibited adenoma organoid growth, suggesting potential therapeutic strategies for intestinal adenomas.

Keywords:
Colon CancerFamilial Adenomatous PolyposisLGR5PROX1

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Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Colorectal cancer is linked to mutations in the Wnt signaling pathway.
  • R-spondins (RSPOs) amplify Wnt signaling in intestinal stem cells and are altered in colorectal tumors.

Purpose of the Study:

  • To investigate the effects of R-spondin 1 (RSPO1) overexpression on tumor development in ApcMin/+ mutant mice.

Main Methods:

  • Adeno-associated viral vectors encoding RSPO1-Fc or control were injected into ApcMin/+ mice.
  • Intestinal crypts were cultured as organoids and treated with RSPO1-Fc and/or a TGFBR inhibitor.
  • Tissues and organoids were analyzed using immunohistochemistry, qPCR, and single-cell RNA sequencing.

Main Results:

  • RSPO1 overexpression in ApcMin/+ mice led to fewer, smaller intestinal tumors and longer survival.
  • RSPO1 increased apoptosis and Wnt target gene expression in adenomas, followed by reduced proliferation.
  • RSPO1 inhibited adenoma organoid growth, an effect reversed by TGFBR inhibition.

Conclusions:

  • RSPO1 expression in ApcMin/+ mice reduces tumor burden by increasing apoptosis and decreasing proliferation.
  • RSPO1 inhibits adenoma organoid growth, with TGFB signaling mediating this effect.
  • Increasing RSPO1 expression may offer a therapeutic strategy for intestinal adenomas.