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Macrocyclic peptides targeting human CD44 inhibit cell adhesion.

Athanasios Chatzopoulos1, Constantinos Kolliopoulos2, Yizhen Yin3

  • 1Department of Medical Biochemistry and Microbiology, Uppsala University, SE-751 23 Uppsala, Sweden; Biochemistry, Biochemical Analysis & Matrix Pathobiology Res. Group, Laboratory of Biochemistry, Department of Chemistry, University of Patras, 26504 Patras, Greece.

Cellular Signalling
|October 24, 2025
PubMed
Summary

Macrocyclic peptides L4-3 and D4-3 inhibit CD44-hyaluronan interactions, reducing glioma cell adhesion and impacting EGFR signaling. These peptides offer potential therapeutic strategies for aggressive tumors by disrupting tumor cell signaling pathways.

Keywords:
CD44Cancer cellsHyaluronanMacrocyclic peptides

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Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • CD44-hyaluronan interactions are crucial in aggressive tumor progression.
  • Glioma, an aggressive cancer, involves complex signaling pathways like EGFR.

Purpose of the Study:

  • To develop novel macrocyclic peptides targeting the CD44-hyaluronan binding domain.
  • To investigate the effects of L4-3 and D4-3 peptides on CD44 signaling in glioma cells and fibroblasts.

Main Methods:

  • Identification of macrocyclic peptides (L4-3, D4-3) that bind to CD44.
  • Inhibition of hyaluronan binding to CD44 in U251MG glioma cells and normal fibroblasts.
  • Analysis of downstream signaling pathways, including EGFR, AKT, and ERK1/2.

Main Results:

  • L4-3 and D4-3 reduced glioma cell adhesion and affected signaling pathways.
  • L4-3 enhanced negative feedback regulation of EGFR and inhibited EGF-mediated AKT activation.
  • D4-3 suppressed hyaluronan-CD44-mediated adhesion in fibroblasts without affecting AKT/ERK1/2.

Conclusions:

  • Macrocyclic peptides targeting CD44-hyaluronan interactions show therapeutic potential.
  • CD44 signaling cross-talks with EGFR signaling in glioma, offering a target for intervention.
  • Peptide effects vary across cell types, indicating context-dependent mechanisms.