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@ARTICLE{Levy:290199,
      author       = {T. Levy and K. Voeltzke and L. Hruby and K. Alasad and Z.
                      Bas and M. T. Snaebjörnsson$^*$ and R. Marciano and K.
                      Scharov and M. Planque and K. Vriens and S. Christen and C.
                      Funk$^*$ and C. Hassiepen and A. Kahler and B. Heider and D.
                      J. Picard$^*$ and J. K. M. Lim and A. Stefanski and K.
                      Bendrin and A. Vargas-Toscano and U. D. Kahlert and K.
                      Stühler and M. Remke$^*$ and M. Elkabets and T.
                      Grünewald$^*$ and A. S. Reichert and S.-M. Fendt and A.
                      Schulze$^*$ and G. Reifenberger$^*$ and B. Rotblat and G.
                      Leprivier},
      title        = {m{TORC}1 regulates cell survival under glucose starvation
                      through 4{EBP}1/2-mediated translational reprogramming of
                      fatty acid metabolism.},
      journal      = {Nature Communications},
      volume       = {15},
      number       = {1},
      issn         = {2041-1723},
      address      = {[London]},
      publisher    = {Nature Publishing Group UK},
      reportid     = {DKFZ-2024-01032},
      pages        = {4083},
      year         = {2024},
      abstract     = {Energetic stress compels cells to evolve adaptive
                      mechanisms to adjust their metabolism. Inhibition of mTOR
                      kinase complex 1 (mTORC1) is essential for cell survival
                      during glucose starvation. How mTORC1 controls cell
                      viability during glucose starvation is not well understood.
                      Here we show that the mTORC1 effectors eukaryotic initiation
                      factor 4E binding proteins 1/2 (4EBP1/2) confer protection
                      to mammalian cells and budding yeast under glucose
                      starvation. Mechanistically, 4EBP1/2 promote NADPH
                      homeostasis by preventing NADPH-consuming fatty acid
                      synthesis via translational repression of Acetyl-CoA
                      Carboxylase 1 (ACC1), thereby mitigating oxidative stress.
                      This has important relevance for cancer, as
                      oncogene-transformed cells and glioma cells exploit the
                      4EBP1/2 regulation of ACC1 expression and redox balance to
                      combat energetic stress, thereby supporting transformation
                      and tumorigenicity in vitro and in vivo. Clinically, high
                      EIF4EBP1 expression is associated with poor outcomes in
                      several cancer types. Our data reveal that the
                      mTORC1-4EBP1/2 axis provokes a metabolic switch essential
                      for survival during glucose starvation which is exploited by
                      transformed and tumor cells.},
      keywords     = {Mechanistic Target of Rapamycin Complex 1: metabolism /
                      Mechanistic Target of Rapamycin Complex 1: genetics /
                      Glucose: metabolism / Acetyl-CoA Carboxylase: metabolism /
                      Acetyl-CoA Carboxylase: genetics / Humans / Adaptor
                      Proteins, Signal Transducing: metabolism / Adaptor Proteins,
                      Signal Transducing: genetics / Fatty Acids: metabolism /
                      Animals / Cell Survival / Cell Cycle Proteins: metabolism /
                      Cell Cycle Proteins: genetics / Mice / NADP: metabolism /
                      Protein Biosynthesis / Phosphoproteins: metabolism /
                      Phosphoproteins: genetics / Oxidative Stress / Cell Line,
                      Tumor / Eukaryotic Initiation Factors: metabolism /
                      Eukaryotic Initiation Factors: genetics},
      cin          = {A410 / B410 / HD01 / ED01},
      ddc          = {500},
      cid          = {I:(DE-He78)A410-20160331 / I:(DE-He78)B410-20160331 /
                      I:(DE-He78)HD01-20160331 / I:(DE-He78)ED01-20160331},
      pnm          = {311 - Zellbiologie und Tumorbiologie (POF4-311)},
      pid          = {G:(DE-HGF)POF4-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:38744825},
      doi          = {10.1038/s41467-024-48386-y},
      url          = {https://inrepo02.dkfz.de/record/290199},
}