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@ARTICLE{Wickstrm:127785,
      author       = {M. Wickström and C. Dyberg and J. Milosevic and C. Einvik
                      and R. Calero and B. Sveinbjörnsson and E. Sandén and A.
                      Darabi and P. Siesjö and M. Kool$^*$ and P. Kogner and N.
                      Baryawno and J. I. Johnsen},
      title        = {{W}nt/β-catenin pathway regulates {MGMT} gene expression
                      in cancer and inhibition of {W}nt signalling prevents
                      chemoresistance.},
      journal      = {Nature Communications},
      volume       = {6},
      issn         = {2041-1723},
      address      = {London},
      publisher    = {Nature Publishing Group},
      reportid     = {DKFZ-2017-03807},
      pages        = {8904 -},
      year         = {2015},
      abstract     = {The DNA repair enzyme O6-methylguanine-DNA
                      methyltransferase (MGMT) is commonly overexpressed in
                      cancers and is implicated in the development of
                      chemoresistance. The use of drugs inhibiting MGMT has been
                      hindered by their haematologic toxicity and inefficiency. As
                      a different strategy to inhibit MGMT we investigated
                      cellular regulators of MGMT expression in multiple cancers.
                      Here we show a significant correlation between Wnt
                      signalling and MGMT expression in cancers with different
                      origin and confirm the findings by bioinformatic analysis
                      and immunofluorescence. We demonstrate Wnt-dependent MGMT
                      gene expression and cellular co-localization between active
                      β-catenin and MGMT. Pharmacological or genetic inhibition
                      of Wnt activity downregulates MGMT expression and restores
                      chemosensitivity of DNA-alkylating drugs in mouse models.
                      These findings have potential therapeutic implications for
                      chemoresistant cancers, especially of brain tumours where
                      the use of temozolomide is frequently used in treatment.},
      keywords     = {2-(4-(2-methylpyridin-4-yl)phenyl)-N-(4-(pyridin-3-yl)phenyl)acetamide
                      (NLM Chemicals) / Antineoplastic Agents (NLM Chemicals) /
                      Benzeneacetamides (NLM Chemicals) / G007-LK (NLM Chemicals)
                      / Heterocyclic Compounds, 3-Ring (NLM Chemicals) / LGK974
                      (NLM Chemicals) / Pyrans (NLM Chemicals) / Pyrazines (NLM
                      Chemicals) / Pyridines (NLM Chemicals) / Sulfones (NLM
                      Chemicals) / Triazoles (NLM Chemicals) / Tumor Suppressor
                      Proteins (NLM Chemicals) / Wnt Proteins (NLM Chemicals) /
                      XAV939 (NLM Chemicals) / beta Catenin (NLM Chemicals) /
                      irinotecan (NLM Chemicals) / Vincristine (NLM Chemicals) /
                      salinomycin (NLM Chemicals) / Dacarbazine (NLM Chemicals) /
                      Doxorubicin (NLM Chemicals) / DNA Modification Methylases
                      (NLM Chemicals) / MGMT protein, human (NLM Chemicals) /
                      Glucose-6-Phosphate Isomerase (NLM Chemicals) / DNA Repair
                      Enzymes (NLM Chemicals) / Celecoxib (NLM Chemicals) /
                      Cisplatin (NLM Chemicals) / Camptothecin (NLM Chemicals) /
                      temozolomide (NLM Chemicals)},
      cin          = {B062},
      ddc          = {500},
      cid          = {I:(DE-He78)B062-20160331},
      pnm          = {312 - Functional and structural genomics (POF3-312)},
      pid          = {G:(DE-HGF)POF3-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:26603103},
      pmc          = {pmc:PMC4674781},
      doi          = {10.1038/ncomms9904},
      url          = {https://inrepo02.dkfz.de/record/127785},
}