title: Parthenolide induces proliferation inhibition and apoptosis of pancreatic cancer cells in vitro.
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.
authors.affiliation: Department of General Surgery, Sir Run Run Shaw Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, PR China.
authors.forename: Jun-Wei
authors.initials: JW
authors.lastname: Liu
authors.forename: Min-Xia
authors.initials: MX
authors.lastname: Cai
authors.forename: Ying
authors.initials: Y
authors.lastname: Xin
authors.forename: Qing-Song
authors.initials: QS
authors.lastname: Wu
authors.forename: Jun
authors.initials: J
authors.lastname: Ma
authors.forename: Po
authors.initials: P
authors.lastname: Yang
authors.forename: Hai-Yang
authors.initials: HY
authors.lastname: Xie
authors.forename: Dong-Sheng
authors.initials: DS
authors.lastname: Huang
mesh_terms: D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology*; D000971:Antineoplastic Combined Chemotherapy Protocols / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects; D015153:Blotting, Western; D053148:Caspase 3 / Q000378:metabolism; D049109:Cell Proliferation / Q000187:drug effects; D005434:Flow Cytometry; D006801:Humans; D007124:Immunoenzyme Techniques; D066298:In Vitro Techniques; D016328:NF-kappa B / Q000037:antagonists & inhibitors; D009361:Neoplasm Invasiveness; D010190:Pancreatic Neoplasms / Q000188:drug therapy* / Q000378:metabolism* / Q000473:pathology; D012333:RNA, Messenger / Q000235:genetics; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012717:Sesquiterpenes / Q000494:pharmacology*; D014407:Tumor Cells, Cultured
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D016328:NF-kappa B; D012333:RNA, Messenger; D012717:Sesquiterpenes; C002669:parthenolide; D053148:Caspase 3