% IMPORTANT: The following is UTF-8 encoded.  This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.

@ARTICLE{Koch:819805,
      author       = {Koch, Katharina and Hartmann, Rudolf and Schröter,
                      Friederike and Kora Suwala, Abigail and Maciaczyk, Donata
                      and Caroline Krüger, Andrea and Willbold, Dieter and
                      Dietrich Kahlert, Ulf and Maciaczyk, Jaroslaw},
      title        = {{R}eciprocal regulation of the cholinic phenotype and
                      epithelial-mesenchymal transition in glioblastoma cells},
      journal      = {OncoTarget},
      volume       = {7},
      number       = {45},
      issn         = {1949-2553},
      address      = {[S.l.]},
      publisher    = {Impact Journals LLC},
      reportid     = {FZJ-2016-05400},
      pages        = {73414-73431},
      year         = {2016},
      abstract     = {Glioblastoma (GBM) is the most malignant brain tumor with
                      very limited therapeutic options. Standard multimodal
                      treatments, including surgical resection and combined
                      radio-chemotherapy do not target the most aggressive subtype
                      of glioma cells, brain tumor stem cells (BTSCs). BTSCs are
                      thought to be responsible for tumor initiation, progression,
                      and relapse. Furthermore, they have been associated with the
                      expression of mesenchymal features as a result of
                      epithelial-mesenchymal transition (EMT) thereby inducing
                      tumor dissemination and chemo resistance. Using high
                      resolution proton nuclear magnetic resonance spectroscopy
                      (1H NMR) on GBM cell cultures we provide evidence that the
                      expression of well-known EMT activators of the ZEB, TWIST
                      and SNAI families and EMT target genes N-cadherin and
                      VIMENTIN is associated with aberrant choline metabolism. The
                      cholinic phenotype is characterized by high intracellular
                      levels of phosphocholine and total choline derivatives and
                      was associated with malignancy in various cancers. Both
                      genetic and pharmacological inhibition of the cardinal
                      choline metabolism regulator choline kinase alpha (CHKα)
                      significantly reduces the cell viability, invasiveness,
                      clonogenicity, and expression of EMT associated genes in GBM
                      cells. Moreover, in some cell lines synergetic cytotoxic
                      effects were observed when combining the standard of care
                      chemotherapeutic temozolomide with the CHKα inhibitor
                      V-11-0711. Taken together, specific inhibition of the
                      enzymatic activity of CHKα is a powerful strategy to
                      suppress EMT which opens the possibility to target
                      chemo-resistant BTSCs through impairing their mesenchymal
                      transdifferentiation. Moreover, the newly identified
                      EMT-oncometabolic network may be helpful to monitor the
                      invasive properties of glioblastomas and the success of
                      anti-EMT therapy.},
      cin          = {ICS-6},
      ddc          = {610},
      cid          = {I:(DE-Juel1)ICS-6-20110106},
      pnm          = {553 - Physical Basis of Diseases (POF3-553)},
      pid          = {G:(DE-HGF)POF3-553},
      typ          = {PUB:(DE-HGF)16},
      UT           = {WOS:000387452100075},
      doi          = {10.18632/oncotarget.12337},
      url          = {https://juser.fz-juelich.de/record/819805},
}