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ANXA1‑derived peptides suppress gastric and colon cancer cell growth by targeting EphA2 degradation

Juan Feng1, Ta Xiao2, Shan-Shan Lu3

  • 1Department of Otolaryngology Head and Neck Surgery, Xiangya Hospital, Central South University, Changsha, Hunan 410008, P.R. China.

International Journal of Oncology
|September 9, 2020
PubMed

Insights

Annexin A1 (ANXA1) stabilizes EphA2, promoting gastric and colon cancer growth. Disrupting this interaction with ANXA1-derived peptides targets EphA2 for degradation, inhibiting cancer cell proliferation and offering a novel therapeutic strategy.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • EphA2 (EPH receptor A2) is a key factor in human cancers and a target for anticancer drug development.
  • Annexin A1 (ANXA1) interaction with EphA2 enhances EphA2 stability by preventing proteasome degradation in gastric and colon cancer cells.

Purpose of the Study:

  • To investigate the role of ANXA1-EphA2 interaction in gastric cancer (GC) and colon cancer (CC) progression.
  • To develop and evaluate ANXA1-derived peptides as potential therapeutic agents targeting EphA2 degradation.

Main Methods:

  • Identification of ANXA1 amino acid residues (20-30 and 28-30) critical for EphA2 binding and stabilization.
  • Design and synthesis of ANXA1-derived peptides (A1(28-30) and A1(20-30)) fused to cell-penetrating peptides.
  • In vitro and in vivo experiments to assess the efficacy of A1(28-30) and A1(20-30) in blocking ANXA1-EphA2 interaction, inducing EphA2 degradation, and suppressing tumor growth.

Main Results:

  • The ANXA1 N-terminal residues 20-30 and 28-30 are essential for binding and stabilizing EphA2.
  • A1(28-30) and A1(20-30) peptides effectively disrupted the ANXA1-EphA2 interaction.
  • These peptides induced EphA2 degradation and significantly suppressed the growth of GC and CC cells in vitro and in mouse models.

Conclusions:

  • ANXA1 binding stabilizes EphA2 in GC and CC cells.
  • Disruption of the ANXA1-EphA2 interaction using ANXA1-derived peptides represents a promising therapeutic strategy for GC and CC by promoting EphA2 degradation.

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