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@ARTICLE{Alborzinia:277470,
      author       = {H. Alborzinia$^*$ and Z. Chen and U. Yildiz$^*$ and F. P.
                      Freitas and F. C. E. Vogel$^*$ and J. P. Varga$^*$ and J.
                      Batani and C. Bartenhagen and W. Schmitz and G. Büchel and
                      B. Michalke and J. Zheng and S. Meierjohann and E. Girardi
                      and E. Espinet and A. F. Flórez and A. F. Dos Santos and N.
                      Aroua$^*$ and T. Cheytan$^*$ and J. Haenlin$^*$ and L.
                      Schlicker$^*$ and T. N. Xavier da Silva$^*$ and A.
                      Przybylla$^*$ and P. Zeisberger$^*$ and G. Superti-Furga and
                      M. Eilers and M. Conrad and M. Fabiano and U. Schweizer and
                      M. Fischer and A. Schulze$^*$ and A. Trumpp$^*$ and J. P.
                      Friedmann Angeli},
      title        = {{LRP}8-mediated selenocysteine uptake is a targetable
                      vulnerability in {MYCN}-amplified neuroblastoma.},
      journal      = {EMBO molecular medicine},
      volume       = {15},
      number       = {8},
      issn         = {1757-4676},
      address      = {Heidelberg},
      publisher    = {EMBO Press},
      reportid     = {DKFZ-2023-01391},
      pages        = {e18014},
      year         = {2023},
      note         = {#EA:A010#LA:A010# / 2023 Aug 7;15(8):e18014},
      abstract     = {Ferroptosis has emerged as an attractive strategy in cancer
                      therapy. Understanding the operational networks regulating
                      ferroptosis may unravel vulnerabilities that could be
                      harnessed for therapeutic benefit. Using CRISPR-activation
                      screens in ferroptosis hypersensitive cells, we identify the
                      selenoprotein P (SELENOP) receptor, LRP8, as a key
                      determinant protecting MYCN-amplified neuroblastoma cells
                      from ferroptosis. Genetic deletion of LRP8 leads to
                      ferroptosis as a result of an insufficient supply of
                      selenocysteine, which is required for the translation of the
                      antiferroptotic selenoprotein GPX4. This dependency is
                      caused by low expression of alternative selenium uptake
                      pathways such as system Xc- . The identification of LRP8 as
                      a specific vulnerability of MYCN-amplified neuroblastoma
                      cells was confirmed in constitutive and inducible LRP8
                      knockout orthotopic xenografts. These findings disclose a
                      yet-unaccounted mechanism of selective ferroptosis induction
                      that might be explored as a therapeutic strategy for
                      high-risk neuroblastoma and potentially other MYCN-amplified
                      entities.},
      keywords     = {ferroptosis (Other) / neuroblastoma (Other) /
                      selenocysteine (Other) / selenoprotein (Other) / synthetic
                      lethality (Other)},
      cin          = {A010 / A410},
      ddc          = {610},
      cid          = {I:(DE-He78)A010-20160331 / 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:37435859},
      doi          = {10.15252/emmm.202318014},
      url          = {https://inrepo02.dkfz.de/record/277470},
}