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@ARTICLE{Liu:127965,
      author       = {L. Liu$^*$ and A. V. Salnikov$^*$ and N. Bauer$^*$ and E.
                      Aleksandrowicz$^*$ and S. Labsch$^*$ and C. Nwaeburu$^*$ and
                      J. Mattern$^*$ and J. Gladkich$^*$ and P. Schemmer and J.
                      Werner and I. Herr$^*$},
      title        = {{T}riptolide reverses hypoxia-induced
                      epithelial-mesenchymal transition and stem-like features in
                      pancreatic cancer by {NF}-κ{B} downregulation.},
      journal      = {International journal of cancer},
      volume       = {134},
      number       = {10},
      issn         = {0020-7136},
      address      = {Bognor Regis},
      publisher    = {Wiley-Liss},
      reportid     = {DKFZ-2017-03987},
      pages        = {2489 - 2503},
      year         = {2014},
      abstract     = {Pancreatic ductal adenocarcinoma (PDA) is one of the most
                      lethal malignancies characterized by an intense tumor stroma
                      with hypoperfused regions, a significant inflammatory
                      response and pronounced therapy resistance. New therapeutic
                      agents are urgently needed. The plant-derived agent
                      triptolide also known as 'thunder god vine' has a long
                      history in traditional Chinese medicine for treatment of
                      rheumatoid arthritis and cancer and is now in a clinical
                      phase II trial for establishing the efficacy against a
                      placebo. The authors mimicked the situation in patient
                      tumors by induction of hypoxia in experimental models of
                      pancreatic cancer stem cells (CSCs) and evaluated the
                      therapeutic effect of triptolide. Hypoxia led to induction
                      of colony and spheroid formation, aldehyde dehydrogenase 1
                      (ALDH1) and NF-κB activity, migratory potential and a
                      switch in morphology to a fibroblastoid phenotype, as well
                      as stem cell- and epithelial-mesenchymal
                      transition-associated protein expression. Triptolide
                      efficiently inhibited hypoxia-induced transcriptional
                      signaling and downregulated epithelial-mesenchymal
                      transition (EMT) and CSC features in established highly
                      malignant cell lines, whereas sensitive cancer cells or
                      nonmalignant cells were less affected. In vivo triptolide
                      inhibited tumor take and tumor growth. In primary CSCs
                      isolated from patient tumors, triptolide downregulated
                      markers of CSCs, proliferation and mesenchymal cells along
                      with upregulation of markers for apoptosis and epithelial
                      cells. This study is the first to show that triptolide
                      reverses EMT and CSC characteristics and therefore may be
                      superior to current chemotherapeutics for treatment of PDA.},
      keywords     = {Antineoplastic Agents, Alkylating (NLM Chemicals) /
                      Biomarkers, Tumor (NLM Chemicals) / Diterpenes (NLM
                      Chemicals) / Epoxy Compounds (NLM Chemicals) / Isoenzymes
                      (NLM Chemicals) / NF-kappa B (NLM Chemicals) / Phenanthrenes
                      (NLM Chemicals) / Proto-Oncogene Proteins c-rel (NLM
                      Chemicals) / triptolide (NLM Chemicals) / aldehyde
                      dehydrogenase 1 (NLM Chemicals) / Retinal Dehydrogenase (NLM
                      Chemicals)},
      cin          = {G403},
      ddc          = {610},
      cid          = {I:(DE-He78)G403-20160331},
      pnm          = {317 - Translational cancer research (POF3-317)},
      pid          = {G:(DE-HGF)POF3-317},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:24615157},
      pmc          = {pmc:PMC4255690},
      doi          = {10.1002/ijc.28583},
      url          = {https://inrepo02.dkfz.de/record/127965},
}