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@ARTICLE{Snaebjrnsson:298171,
      author       = {M. T. Snaebjörnsson$^*$ and P. Poeller$^*$ and D. Komkova
                      and F. Röhrig and L. Schlicker$^*$ and A. Winkelkotte$^*$
                      and A. B. Chaves-Filho$^*$ and K. M. Al-Shami$^*$ and C. D.
                      Caballero$^*$ and I. Koltsaki$^*$ and F. C. E. Vogel$^*$ and
                      R. C. Frias-Soler$^*$ and R. Rudalska and J. D. Schwarz and
                      E. Wolf and D. Dauch and R. Steuer and A. Schulze$^*$},
      title        = {{T}argeting aldolase {A} in hepatocellular carcinoma leads
                      to imbalanced glycolysis and energy stress due to
                      uncontrolled {FBP} accumulation.},
      journal      = {Nature metabolism},
      volume       = {7},
      number       = {2},
      issn         = {2522-5812},
      address      = {[London]},
      publisher    = {Springer Nature},
      reportid     = {DKFZ-2025-00190},
      pages        = {348-366},
      year         = {2025},
      note         = {#EA:A410#LA:A410# / 2025 Feb;7(2):348-366},
      abstract     = {Increased glycolytic flux is a hallmark of cancer; however,
                      an increasing body of evidence indicates that glycolytic ATP
                      production may be dispensable in cancer, as metabolic
                      plasticity allows cancer cells to readily adapt to
                      disruption of glycolysis by increasing ATP production via
                      oxidative phosphorylation. Using functional genomic
                      screening, we show here that liver cancer cells show a
                      unique sensitivity toward aldolase A (ALDOA) depletion.
                      Targeting glycolysis by disrupting the catalytic activity of
                      ALDOA led to severe energy stress and cell cycle arrest in
                      murine and human hepatocellular carcinoma cell lines. With a
                      combination of metabolic flux analysis, metabolomics,
                      stable-isotope tracing and mathematical modelling, we
                      demonstrate that inhibiting ALDOA induced a state of
                      imbalanced glycolysis in which the investment phase outpaced
                      the payoff phase. Targeting ALDOA effectively converted
                      glycolysis from an energy producing into an energy-consuming
                      process. Moreover, we found that depletion of ALDOA extended
                      survival and reduced cancer cell proliferation in an animal
                      model of hepatocellular carcinoma. Thus, our findings
                      indicate that induction of imbalanced glycolysis by
                      targeting ALDOA presents a unique opportunity to overcome
                      the inherent metabolic plasticity of cancer cells.},
      cin          = {A410},
      ddc          = {610},
      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:39833612},
      doi          = {10.1038/s42255-024-01201-w},
      url          = {https://inrepo02.dkfz.de/record/298171},
}