Inhibitory effect of cucurbitacin E on pancreatic cancer cells growth via STAT3 signaling

J Cancer Res Clin Oncol. 2010 Apr;136(4):603-10. doi: 10.1007/s00432-009-0698-x. Epub 2009 Oct 9.

Abstract

Purpose: Pancreatic cancer has been a serious disease worldwide for its high mortality. Cucurbitacin E is a member of triterpenoid family isolated from plants showing antiproliferative activity on various cancer cells. In this study, we have explored whether cucurbitacin E also has an anti-tumor effect on pancreatic cancer cells.

Methods: Human pancreatic cancer cells PANC-1 were used to explore the effect and possible mechanisms of cucurbitacin E on cell cycle progression, apoptosis and proliferation.

Results: Cucurbitacin E has inhibited the growth of PANC-1 cells in a dose- and time-dependent manner, and has caused accumulation of cells at the G(2)/M phase as well as apoptosis. Western blotting also showed that cucurbitacin E treatment can inhibit STAT3 phosphorylation while upregulate p53 expression.

Conclusions: Our results suggested that cucurbitacin E may be an effective regimen for the chemotherapy of pancreatic cancer.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antineoplastic Agents / pharmacology*
  • Antineoplastic Agents / therapeutic use
  • Apoptosis
  • Cell Cycle
  • Cell Line, Tumor
  • Cell Proliferation
  • Dose-Response Relationship, Drug
  • Humans
  • Pancreas / drug effects
  • Pancreas / metabolism
  • Pancreas / pathology
  • Pancreatic Neoplasms / drug therapy*
  • Pancreatic Neoplasms / metabolism
  • Pancreatic Neoplasms / pathology
  • STAT3 Transcription Factor / metabolism*
  • Signal Transduction*
  • Triterpenes / pharmacology*
  • Triterpenes / therapeutic use

Substances

  • Antineoplastic Agents
  • STAT3 Transcription Factor
  • Triterpenes
  • cucurbitacin E