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AdipoRon Attenuates Wnt Signaling by Reducing Cholesterol-Dependent Plasma Membrane Rigidity.

Michael L Salinas1, Natividad R Fuentes2, Rachel Choate3

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Adiponectin signaling, reduced in obesity, may protect against colon cancer by altering cell membrane properties. This pathway impacts cholesterol levels and Wnt signaling, potentially explaining obesity-driven cancer risks.

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Area of Science:

  • Oncology
  • Cell Biology
  • Metabolism

Background:

  • Obesity is linked to increased colorectal cancer risk.
  • Adiponectin, an adipokine reduced in obesity, has shown protective effects against colon cancer.
  • Previous studies indicated adiponectin and its agonist AdipoRon reduce Lgr5+ stem cells, but the mechanism is unclear.

Purpose of the Study:

  • To investigate how adiponectin signaling influences colon cancer risk by modulating plasma membrane biophysical properties.
  • To determine the effect of AdipoRon on Wnt-driven signaling and colonic stem cell proliferation.

Main Methods:

  • Utilized physicochemical sensitive dyes (Di-4-ANEPPDHQ, C-laurdan) to assess plasma membrane rigidity.
  • Employed LEF luciferase reporter assay to measure Wnt-driven signaling.
  • Assessed colonic organoid proliferation to evaluate cell growth.

Main Results:

  • AdipoRon treatment decreased the rigidity of the colonic cell plasma membrane.
  • This decrease in membrane rigidity correlated with reduced free cholesterol in the plasma membrane and its accumulation in lysosomes.
  • Adiponectin receptor activation modulated cellular cholesterol homeostasis and Wnt-driven signaling.

Conclusions:

  • Adiponectin signaling influences colon cancer progression by altering plasma membrane biophysical properties and cholesterol homeostasis.
  • These findings provide insights into the mechanisms by which obesity may promote colon cancer.
  • Targeting adiponectin signaling could offer novel therapeutic strategies for obesity-related colorectal cancer.