Endostar attenuates melanoma tumor growth via its interruption of b-FGF mediated angiogenesis

Lijia Xiao1, ShuCai Yang2, Jianhua Hao1

  • 1Department of Clinical Laboratory, Nanshan affiliated Hospital of Guangdong Medical College, Shenzhen 518052, China.

Cancer Letters
|January 20, 2015
PubMed

Insights

Endostar effectively inhibits melanoma tumor growth by blocking fibroblast growth factor-induced (b-FGF) angiogenesis. This peptide drug targets the MAPK signaling pathway, showing potential for melanoma treatment.

Area of Science:

  • Oncology
  • Angiogenesis Research
  • Pharmacology

Background:

  • Fibroblast growth factors (b-FGF) are key inducers of angiogenesis, making them potential therapeutic targets in melanoma.
  • Endostar, a peptide drug, has demonstrated efficacy in non-small cell lung cancer but its role in melanoma is unexplored.

Purpose of the Study:

  • To investigate the anti-angiogenic and anti-tumor effects of Endostar in melanoma.
  • To elucidate the mechanism of Endostar's action on b-FGF-induced angiogenesis and signaling pathways.

Main Methods:

  • In vivo studies using a mouse melanoma model to assess tumor growth, micro-vessel density, and serum b-FGF levels.
  • In vitro experiments on human umbilical vein endothelial cells (HUVECs) to evaluate proliferation, migration, tube formation, and MAPK pathway activation (p38, ERK1/2).

Main Results:

  • Endostar treatment significantly inhibited melanoma tumor growth and reduced micro-vessel density and serum b-FGF levels in vivo.
  • In vitro, Endostar dose-dependently decreased HUVEC proliferation, migration, and tube formation.
  • Endostar treatment attenuated b-FGF-induced phosphorylation of p38 and ERK1/2 in HUVECs.

Conclusions:

  • Endostar exerts anti-tumor effects in melanoma by suppressing b-FGF-induced angiogenesis.
  • The drug's mechanism involves inhibiting the b-FGF-activated MAPK signaling pathway.
  • Endostar presents a potential therapeutic option for clinical melanoma treatment.

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