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Updated: Jan 27, 2026

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Published on: December 9, 2025

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Suppression of migratory and metastatic pathways via blocking VEGFR1 and VEGFR2

Afsaneh Sadremomtaz1, Farzad Kobarfard2, Kamran Mansouri3

  • 1a Department of Biology, Faculty of Sciences , University of Guilan , Rasht , Iran.

Journal of Receptor and Signal Transduction Research
|April 2, 2019
PubMed
Abstract

Insights

A novel peptide (VGB) effectively inhibits tumor growth and metastasis by blocking vascular endothelial growth factor receptors (VEGFR1/VEGFR2). This dual blockade targets key mediators of angiogenesis, proliferation, and epithelial-mesenchymal transition (EMT).

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Vascular Endothelial Growth Factor (VEGF) A and B are key drivers of tumor angiogenesis, metastasis, and epithelial-mesenchymal transition (EMT) through VEGFR1/VEGFR2 signaling.
  • Targeting these interactions offers a potential strategy to inhibit tumor progression.

Purpose of the Study:

  • To investigate the inhibitory effects of a novel peptide (VGB) targeting both VEGFR1 and VEGFR2.
  • To assess VGB's impact on VEGF-induced endothelial cell proliferation, migration, and downstream signaling pathways involved in metastasis.

Main Methods:

  • A 14-mer peptide (VGB) was designed to recognize both VEGFR1 and VEGFR2.
  • In vitro assays (MTT, scratch assay) evaluated proliferation and migration.
  • Quantitative real-time PCR and immunohistochemistry (IHC) assessed downstream gene and protein expression in tumors.

Main Results:

  • VGB inhibited VEGF-induced proliferation of HUVECs, 4T1, and U87 cells in a dose- and time-dependent manner.
  • VGB suppressed metastasis-related mediators including MMP-9, c-Myc, and NF-κβ, while increasing E-cadherin expression in vivo.
  • Tumor treatment with VGB reduced p-AKT, p-ERK1/2, MMP-9, and NF-κβ, and increased E-cadherin.

Conclusions:

  • Simultaneous blockade of VEGFR1/VEGFR2 using VGB is a promising strategy against solid tumors.
  • VGB effectively targets multiple mediators of tumor angiogenesis, growth, and metastasis.
Keywords:
VEGFR1VEGFR2angiogenesismetastasismigration

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