Novel peptides suppress VEGFR-3 activity and antagonize VEGFR-3-mediated oncogenic effects

Yi Wen Chang, Chih Ming Su, Yen-Hao Su, Yuan Soon Ho, Hui Huang Lai, Hsin An Chen, Min Liang Kuo, Wen Chun Hung, Ya Wen Chen, Chih Hsiung Wu, Pai Sheng Chen, Jen Liang Su

Research output: Contribution to journalArticlepeer-review

19 Citations (Scopus)


Vascular endothelial growth factor receptor 3 (VEGFR-3) supports tumor lymphangiogenesis. It was originally identified as a lymphangiogenic factor expressed in lymphatic endothelial cells. VEGFR-3 was detected in advanced human malignancies and correlated with poor prognosis. Our previous studies show that activation of the VEGF-C/VEGFR-3 axis promotes cancer metastasis and is associated with clinical progression in patients with lung cancer, indicating that VEGFR-3 is a potential target for cancer therapy. In this study, we developed eight peptides targeting VEGFR-3. Two peptides strongly inhibited the kinase activity of VEGFR-3 and suppressed VEGF-C-mediated invasion of cancer cells. Moreover, these peptides abolished VEGF-C-induced drug resistance and tumor initiating cell formation. This study demonstrates the therapeutic potential of VEGFR-3-targeting peptides.

Original languageEnglish
Pages (from-to)3823-3835
Number of pages13
Issue number11
Publication statusPublished - 2014


  • Drug resistance
  • Metastasis
  • VEGFR-3
  • VEGFR-3-targeting peptides

ASJC Scopus subject areas

  • Oncology

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