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@ARTICLE{SaineroAlcolado:287681,
      author       = {L. Sainero-Alcolado and E. Garde-Lapido and M. T.
                      Snaebjörnsson$^*$ and S. Schoch and I. Stevens and M. V.
                      Ruiz-Pérez and C. Dyrager and V. Pelechano and H. Axelson
                      and A. Schulze$^*$ and M. Arsenian-Henriksson},
      title        = {{T}argeting {MYC} induces lipid droplet accumulation by
                      upregulation of {HILPDA} in clear cell renal cell
                      carcinoma.},
      journal      = {Proceedings of the National Academy of Sciences of the
                      United States of America},
      volume       = {121},
      number       = {7},
      issn         = {0027-8424},
      address      = {Washington, DC},
      publisher    = {National Acad. of Sciences},
      reportid     = {DKFZ-2024-00309},
      pages        = {e2310479121},
      year         = {2024},
      abstract     = {Metabolic reprogramming is critical during clear cell renal
                      cell carcinoma (ccRCC) tumorigenesis, manifested by
                      accumulation of lipid droplets (LDs), organelles that have
                      emerged as new hallmarks of cancer. Yet, regulation of their
                      biogenesis is still poorly understood. Here, we demonstrate
                      that MYC inhibition in ccRCC cells lacking the von Hippel
                      Lindau (VHL) gene leads to increased triglyceride content
                      potentiating LD formation in a glutamine-dependent manner.
                      Importantly, the concurrent inhibition of MYC signaling and
                      glutamine metabolism prevented LD accumulation and reduced
                      tumor burden in vivo. Furthermore, we identified the
                      hypoxia-inducible lipid droplet-associated protein (HILPDA)
                      as the key driver for induction of MYC-driven LD
                      accumulation and demonstrated that conversely,
                      proliferation, LD formation, and tumor growth are impaired
                      upon its downregulation. Finally, analysis of ccRCC tissue
                      as well as healthy renal control samples postulated HILPDA
                      as a specific ccRCC biomarker. Together, these results
                      provide an attractive approach for development of
                      alternative therapeutic interventions for the treatment of
                      this type of renal cancer.},
      keywords     = {HILPDA (Other) / MYC (Other) / clear cell renal cell
                      carcinoma (Other) / glutamine (Other) / lipid droplets
                      (Other)},
      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:38335255},
      doi          = {10.1073/pnas.2310479121},
      url          = {https://inrepo02.dkfz.de/record/287681},
}