Parthenolide induces proliferation inhibition and apoptosis of pancreatic cancer cells in vitro

J Exp Clin Cancer Res. 2010 Aug 10;29(1):108. doi: 10.1186/1756-9966-29-108.

Abstract

Background: To explore the anti-tumor effects of parthenolide in human pancreatic cancer.

Methods: BxPC-3 cell, a human pancreatic cancer, was treated with parthenolide at different concentrations. The MTT assay was used to analyze cell viability. Flow cytometry and DNA fragmentation analysis were applied to evaluate apoptosis after parthenolide treatment. The wound closure and cell invasion assay were also employed in the study. Western blotting was used to demonstrate Bad, Bcl-2, Bax, caspase-9 and pro-caspase-3 expression.

Results: The MTT assay indicated that the pancreatic cancer growth could be dose-dependently inhibited by parthenoolide. This phenomenon was confirmed by flow cytometry and DNA fragmentation analysis. The wound closure assay and cell invasion assay showed that BxPC-3 cell was significantly suppressed by parthenolide at 7.5 microM and 15 microM. Western Blotting demonstrated the Bcl-2 and pro-caspase-3 were down-regulated while the Bax and caspase-9 were up-regulated. No alteration in Bad expression was found after treatment.

Conclusions: The parthenolide can inhibit the cell growth, migration, and induce the apoptosis in human pancreatic cancer. These findings may provide a novel approach for pancreatic cancer treatment.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Anti-Inflammatory Agents, Non-Steroidal / pharmacology*
  • Antineoplastic Combined Chemotherapy Protocols / pharmacology*
  • Apoptosis / drug effects
  • Blotting, Western
  • Caspase 3 / metabolism
  • Cell Proliferation / drug effects
  • Flow Cytometry
  • Humans
  • Immunoenzyme Techniques
  • In Vitro Techniques
  • NF-kappa B / antagonists & inhibitors
  • Neoplasm Invasiveness
  • Pancreatic Neoplasms / drug therapy*
  • Pancreatic Neoplasms / metabolism*
  • Pancreatic Neoplasms / pathology
  • RNA, Messenger / genetics
  • Reverse Transcriptase Polymerase Chain Reaction
  • Sesquiterpenes / pharmacology*
  • Tumor Cells, Cultured

Substances

  • Anti-Inflammatory Agents, Non-Steroidal
  • NF-kappa B
  • RNA, Messenger
  • Sesquiterpenes
  • parthenolide
  • Caspase 3