Particle.news

Download on the App Store

Benzaldehyde Disrupts Protein Interface to Thwart Pancreatic Cancer Resistance and Metastasis

Preclinical research shows blocking a key protein interaction restores treatment sensitivity in resistant pancreatic tumors

Image

Overview

  • The compound targets the interface between 14-3-3ζ and Ser28-phosphorylated histone H3, blocking expression of genes that drive treatment resistance and epithelial-to-mesenchymal plasticity.
  • In cell cultures, benzaldehyde halted growth of pancreatic cancer cells resistant to radiation and the tyrosine kinase inhibitor osimertinib and enhanced the effects of radiotherapy.
  • In mouse models, a benzaldehyde derivative reduced tumor size and prevented lung metastases by suppressing epithelial-to-mesenchymal transition.
  • Dr. Hideyuki Saya and colleagues at Fujita Health University detailed the molecular mechanism in a study published May 2 in the British Journal of Cancer.
  • Researchers propose developing benzaldehyde-based agents alongside existing targeted therapies to overcome clinical resistance in pancreatic cancer.