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MOMAST® Downregulates AQP3 Expression and Function in Human Colon Cells.

Ines Angelini1, Mariangela Centrone1, Giusy Rita Caponio1

  • 1Department of Biosciences, Biotechnologies, and Environment, University of Bari "Aldo Moro", 70125 Bari, Italy.

Antioxidants (Basel, Switzerland)
|January 25, 2025
PubMed
Summary

MOMAST®, an olive wastewater complex, reduces colon cell viability and AQP3 expression. This antioxidant inhibits glycerol and H2O2 uptake, suggesting potential for colon disease treatment.

Keywords:
AQP3EMTMOMAST®colon cellspolyphenolsvimentinwaste and by-products

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Area of Science:

  • Cell Biology
  • Molecular Biology
  • Gastroenterology

Background:

  • Aquaglyceroporin 3 (AQP3) facilitates water, glycerol, and hydrogen peroxide transport in human colon cells.
  • Aberrant AQP3 expression is linked to diseases with abnormal cell growth and proliferation.
  • MOMAST®, a patented antioxidant from olive wastewater, is investigated for its effects on colon cells.

Purpose of the Study:

  • To evaluate the effects of MOMAST® on human colon HCT8 cells.
  • To investigate MOMAST®'s impact on AQP3 expression and function.
  • To explore MOMAST®'s potential as an adjuvant therapy for colon diseases.

Main Methods:

  • Cell viability assays were performed on HCT8 cells treated with MOMAST®.
  • Confocal microscopy and Western Blotting were used to assess AQP3 expression.
  • Functional studies measured glycerol and H2O2 uptake, alongside epithelial-mesenchymal transition (EMT) markers.

Main Results:

  • MOMAST® treatment reduced HCT8 cell viability.
  • Significant downregulation of AQP3 expression and protein levels was observed.
  • MOMAST® decreased glycerol and H2O2 uptake, and reduced levels of EMT markers like vimentin and β-catenin.

Conclusions:

  • MOMAST® effectively reduces colon cell viability and AQP3-mediated transport.
  • The observed decrease in AQP3 correlates with reduced glycerol and H2O2 uptake.
  • MOMAST® shows promise as an adjuvant therapy for colon diseases characterized by abnormal cell growth, by targeting AQP3.