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

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.
AuthorsJia Qi, Ge Xia, Cheng Rong Huang, Jian Xia Wang, Jian Zhang
JournalThe American journal of Chinese medicine (Am J Chin Med) Vol. 43 Issue 2 Pg. 337-47 ( 2015) ISSN: 1793-6853 [Electronic] Singapore
PMID25787299 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • STAT3 Transcription Factor
  • STAT3 protein, human
  • Triterpenes
  • Vascular Endothelial Growth Factor A
  • cucurbitacin I
Topics
  • Autocrine Communication (drug effects)
  • Breast Neoplasms (blood supply, genetics, 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, physiology)
  • Signal Transduction (drug effects)
  • Transcription, Genetic (drug effects)
  • Triterpenes (pharmacology, therapeutic use)
  • Tumor Microenvironment (drug effects, genetics)
  • Vascular Endothelial Growth Factor A (genetics)

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