[Inhibitory effect of cantharidin on invasion and metastasis of highly metastatic ovarian carcinoma cell line HO-8910PM]

Ai Zheng. 2005 Apr;24(4):443-7.
[Article in Chinese]

Abstract

Background & objective: Cantharidin, a natural toxin, has specific antitumor actions. Many researches confirmed that nuclear factor-kappaB (NF-kappaB) closely relates with invasion and metastasis of tumor. This study was designed to investigate inhibitory effect of cantharidin on metastasis-related ability of human highly metastatic ovarian carcinoma cell line HO-8910PM, and its mechanism.

Methods: MTT assay was used to examine cytotoxicity of cantharidin on HO-8910PM cells. Effect of cantharidin on adhesion potential of HO-8910PM cells was tested by cell-Matrigel adhesion assay. Transwell chamber assay was performed to determine its effect on invasion and migration capacities of HO-8910PM cells. Protein levels of NF-kappaB P65 subunit and vascular endothelial growth factor (VEGF) were assessed by Western blot.

Results: After 6-h treatment of 20 micromol/L of cantharidin, inhibitory rate of HO-8910PM cells was (8.4+/-2.2)%, inhibitory rates of invasion, migration, and adhesion capacities of HO-8910PM cells were (38.8+/-1.7)%, (40.3+/-5.6)%, and (55.1+/-6.7)%, respectively; protein levels of NF-kappaB P65 subunit and VEGF were down-regulated.

Conclusions: Cantharidin can inhibit migration, invasion, and adhesion of HO-8910PM cells. Its possible mechanism may be involved in down-regulations of NF-kappaB P65 subunit and VEGF.

Publication types

  • English Abstract
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antineoplastic Agents / pharmacology*
  • Cantharidin / pharmacology*
  • Cell Adhesion / drug effects
  • Cell Line, Tumor
  • Cell Movement / drug effects*
  • Cell Proliferation / drug effects
  • Down-Regulation
  • Female
  • Humans
  • Neoplasm Invasiveness
  • Neoplasm Metastasis
  • Ovarian Neoplasms / metabolism
  • Ovarian Neoplasms / pathology*
  • Transcription Factor RelA / metabolism*
  • Vascular Endothelial Growth Factor A / metabolism*

Substances

  • Antineoplastic Agents
  • Transcription Factor RelA
  • Vascular Endothelial Growth Factor A
  • Cantharidin