JSI-124 (Cucurbitacin I) inhibits tumor angiogenesis of human breast cancer through reduction of STAT3 phosphorylation

Am J Chin Med. 2015;43(2):337-47. doi: 10.1142/S0192415X15500226. Epub 2015 Mar 19.

Abstract

Breast cancer (BC) is the most frequently diagnosed type of cancer all over the world. Angiogenesis, a physiological or pathological process characterized by the sprouting of new blood vessels from existing vessels, plays a vital role in tumor nutrition. In this work, we used JSI-124 (Cucurbitacin I), a selective JAK/STAT3 signaling pathway inhibitor, to investigate the role of STAT3 in tumor angiogenesis of a human BC cell line in vitro. JSI-124 inhibited cell viability, proliferation, adhesion, migration and tube formation of a human BC cell line MDA-MB-468. After transfection with pMXs-Stat3C, a dominant active mutant, the inhibitory effects of JSI-124 on MDA-MB-468 were abolished. Furthermore, JSI-124 reduced the phosphorylation of STAT3. These results suggested that JSI-124 inhibited tumor angiogenesis of the human BC cell line in vitro through the reduction of STAT3 phosphorylation. In addition, JSI-124 could reduce VEGF transcription and secretion, suggesting that JSI-124 is also involved in the inhibition of the VEGF autocrine loop in the tumor microenvironment.

Keywords: Angiogenesis; Breast Cancer; JSI-124; STAT3 Inhibitor.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Autocrine Communication / drug effects
  • Breast Neoplasms / blood supply*
  • Breast Neoplasms / genetics*
  • Breast Neoplasms / pathology
  • Cell Adhesion / drug effects
  • Cell Line, Tumor
  • Cell Movement / drug effects
  • Cell Survival / drug effects
  • Cell Transformation, Neoplastic / drug effects
  • Depression, Chemical
  • Female
  • Humans
  • Molecular Targeted Therapy
  • Neovascularization, Pathologic / drug therapy*
  • Phosphorylation / drug effects
  • Phytotherapy*
  • STAT3 Transcription Factor / metabolism
  • STAT3 Transcription Factor / physiology*
  • Signal Transduction / drug effects*
  • Transcription, Genetic / drug effects
  • Triterpenes / pharmacology*
  • Triterpenes / therapeutic use*
  • Tumor Microenvironment / drug effects
  • Tumor Microenvironment / genetics
  • Vascular Endothelial Growth Factor A / genetics

Substances

  • STAT3 Transcription Factor
  • STAT3 protein, human
  • Triterpenes
  • Vascular Endothelial Growth Factor A
  • cucurbitacin I