% 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{Phillips:130329,
      author       = {E. Phillips$^*$ and V. Lang$^*$ and J. Bohlen$^*$ and F.
                      Bethke$^*$ and L. Puccio$^*$ and D. Tichy$^*$ and C.
                      Herold-Mende$^*$ and T. Hielscher$^*$ and P. Lichter$^*$ and
                      V. Goidts$^*$},
      title        = {{T}argeting atypical protein kinase {C} iota reduces
                      viability in glioblastoma stem-like cells via a notch
                      signaling mechanism.},
      journal      = {International journal of cancer},
      volume       = {139},
      number       = {8},
      issn         = {0020-7136},
      address      = {Bognor Regis},
      publisher    = {Wiley-Liss},
      reportid     = {DKFZ-2017-05408},
      pages        = {1776 - 1787},
      year         = {2016},
      abstract     = {In a previous study, Protein Kinase C iota (PRKCI) emerged
                      as an important candidate gene for glioblastoma (GBM)
                      stem-like cell (GSC) survival. Here, we show that PKCι is
                      overexpressed and activated in patient derived GSCs compared
                      with normal neural stem cells and normal brain lysate, and
                      that silencing of PRKCI in GSCs causes apoptosis, along with
                      loss of clonogenicity and reduced proliferation. Notably,
                      PRKCI silencing reduces tumor growth in vivo in a xenograft
                      mouse model. PKCι has been intensively studied as a
                      therapeutic target in non-small cell lung cancer, resulting
                      in the identification of an inhibitor, aurothiomalate (ATM),
                      which disrupts the PKCι/ERK signaling axis. However, we
                      show that, although sensitive to pharmacological inhibition
                      via a pseudosubstrate peptide inhibitor, GSCs are much less
                      sensitive to ATM, suggesting that PKCι acts along a
                      different signaling axis in GSCs. Gene expression profiling
                      of PRKCI-silenced GSCs revealed a novel role of the Notch
                      signaling pathway in PKCι mediated GSC survival. A
                      proximity ligation assay showed that Notch1 and PKCι are in
                      close proximity in GSCs. Targeting PKCι in the context of
                      Notch signaling could be an effective way of attacking the
                      GSC population in GBM.},
      keywords     = {Isoenzymes (NLM Chemicals) / Protein Kinase Inhibitors (NLM
                      Chemicals) / Receptors, Notch (NLM Chemicals) / Protein
                      Kinase C (NLM Chemicals) / protein kinase C lambda (NLM
                      Chemicals)},
      cin          = {B067 / B060 / C060},
      ddc          = {610},
      cid          = {I:(DE-He78)B067-20160331 / I:(DE-He78)B060-20160331 /
                      I:(DE-He78)C060-20160331},
      pnm          = {312 - Functional and structural genomics (POF3-312)},
      pid          = {G:(DE-HGF)POF3-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:27299852},
      doi          = {10.1002/ijc.30234},
      url          = {https://inrepo02.dkfz.de/record/130329},
}