Betulinic acid suppresses NGAL-induced epithelial-to-mesenchymal transition in melanoma

Dorina Gheorgheosu1, Michaela Jung, Bilge Ören

  • 1Department of Pathophysiology, Victor Babes University of Medicine and Pharmacy, 300041 Timisoara, Romania.

Biological Chemistry
|February 13, 2013
PubMed

Insights

Betulinic acid (BA) inhibits melanoma cell invasion by blocking epithelial-to-mesenchymal transition (EMT). This study shows BA reduces mesenchymal markers and suppresses NGAL-induced EMT, offering a potential therapeutic strategy.

Area of Science:

  • Oncology
  • Cancer Biology
  • Molecular Medicine

Background:

  • Betulinic acid (BA) demonstrates antitumoral properties, including inhibition of proliferation, invasion, and angiogenesis.
  • Epithelial-to-mesenchymal transition (EMT) is a critical process in cancer metastasis.
  • Neutrophil gelatinase-associated lipocalin (NGAL) is implicated in inducing EMT, but BA's effect on this process is unknown.

Purpose of the Study:

  • To investigate the effect of Betulinic acid (BA) on NGAL-induced epithelial-to-mesenchymal transition (EMT) in melanoma cells.
  • To determine if BA can reverse or inhibit the EMT process and associated invasive phenotypes.

Main Methods:

  • A375 melanoma cells were treated with Betulinic acid (BA).
  • Analysis included monitoring of epithelial and mesenchymal markers, cytoskeletal organization, and NGAL production.
  • EMT was induced both endogenously and exogenously using NGAL.

Main Results:

  • Betulinic acid (BA) downregulated mesenchymal markers and upregulated epithelial markers in A375 melanoma cells.
  • BA inhibited cytoskeletal reorganization and limited endogenous NGAL production.
  • BA suppressed NGAL-induced EMT and reduced the invasive cellular phenotype.

Conclusions:

  • Betulinic acid (BA) interferes with EMT-associated changes in melanoma cells.
  • BA antagonizes melanoma cell invasion by modulating EMT pathways.
  • These findings suggest BA as a potential therapeutic agent against invasive melanoma.

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