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@ARTICLE{Kalogirou:170397,
      author       = {C. Kalogirou and J. Linxweiler and P. Schmucker and M. T.
                      Snaebjornsson$^*$ and W. Schmitz and S. Wach and M. Krebs
                      and E. Hartmann and M. Puhr and A. Müller and M. Spahn and
                      A. K. Seitz and T. Frank and H. Marouf and G. Büchel and M.
                      Eckstein and H. Kübler and M. Eilers and M. Saar and K.
                      Junker and F. Röhrig and B. Kneitz and M. T. Rosenfeldt and
                      A. Schulze$^*$},
      title        = {{M}i{R}-205-driven downregulation of cholesterol
                      biosynthesis through {SQLE}-inhibition identifies
                      therapeutic vulnerability in aggressive prostate cancer.},
      journal      = {Nature Communications},
      volume       = {12},
      number       = {1},
      issn         = {2041-1723},
      address      = {[London]},
      publisher    = {Nature Publishing Group UK},
      reportid     = {DKFZ-2021-01906},
      pages        = {5066},
      year         = {2021},
      note         = {#LA:A410#},
      abstract     = {Prostate cancer (PCa) shows strong dependence on the
                      androgen receptor (AR) pathway. Here, we show that squalene
                      epoxidase (SQLE), an enzyme of the cholesterol biosynthesis
                      pathway, is overexpressed in advanced PCa and its expression
                      correlates with poor survival. SQLE expression is controlled
                      by micro-RNA 205 (miR-205), which is significantly
                      downregulated in advanced PCa. Restoration of miR-205
                      expression or competitive inhibition of SQLE led to
                      inhibition of de novo cholesterol biosynthesis. Furthermore,
                      SQLE was essential for proliferation of AR-positive PCa cell
                      lines, including abiraterone or enzalutamide resistant
                      derivatives, and blocked transactivation of the AR pathway.
                      Inhibition of SQLE with the FDA approved antifungal drug
                      terbinafine also efficiently blocked orthotopic tumour
                      growth in mice. Finally, terbinafine reduced levels of
                      prostate specific antigen (PSA) in three out of four
                      late-stage PCa patients. These results highlight SQLE as a
                      therapeutic target for the treatment of advanced PCa.},
      cin          = {A410},
      ddc          = {500},
      cid          = {I:(DE-He78)A410-20160331},
      pnm          = {311 - Zellbiologie und Tumorbiologie (POF4-311)},
      pid          = {G:(DE-HGF)POF4-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:34417456},
      doi          = {10.1038/s41467-021-25325-9},
      url          = {https://inrepo02.dkfz.de/record/170397},
}