% IMPORTANT: The following is UTF-8 encoded.  This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.

@ARTICLE{Lee:166539,
      author       = {W. D. Lee and A. C. Pirona$^*$ and B. Sarvin and A. Stern
                      and K. Nevo-Dinur and E. Besser and N. Sarvin and S. Lagziel
                      and D. Mukha and S. Raz and E. Aizenshtein and T. Shlomi},
      title        = {{T}umor {R}eliance on {C}ytosolic versus {M}itochondrial
                      {O}ne-{C}arbon {F}lux {D}epends on {F}olate {A}vailability.},
      journal      = {Cell metabolism},
      volume       = {33},
      number       = {1},
      issn         = {1550-4131},
      address      = {Cambridge, Mass.},
      publisher    = {Cell Press},
      reportid     = {DKFZ-2020-02982},
      pages        = {190-198.e6},
      year         = {2021},
      note         = {2021 Jan 5;33(1):190-198.e6 / #DKFZ-MOST-Ca173#},
      abstract     = {Folate metabolism supplies one-carbon (1C) units for
                      biosynthesis and methylation and has long been a target for
                      cancer chemotherapy. Mitochondrial serine catabolism is
                      considered the sole contributor of folate-mediated 1C units
                      in proliferating cancer cells. Here, we show that under
                      physiological folate levels in the cell environment,
                      cytosolic serine-hydroxymethyltransferase (SHMT1) is the
                      predominant source of 1C units in a variety of cancers,
                      while mitochondrial 1C flux is overly repressed.
                      Tumor-specific reliance on cytosolic 1C flux is associated
                      with poor capacity to retain intracellular folates, which is
                      determined by the expression of SLC19A1, which encodes the
                      reduced folate carrier (RFC). We show that silencing SHMT1
                      in cells with low RFC expression impairs pyrimidine
                      biosynthesis and tumor growth in vivo. Overall, our
                      findings reveal major diversity in cancer cell utilization
                      of the cytosolic versus mitochondrial folate cycle across
                      tumors and SLC19A1 expression as a marker for increased
                      reliance on SHMT1.},
      keywords     = {SHMT (Other) / cancer metabolism (Other) / folate cycle
                      (Other) / in vivo (Other) / isotope tracing (Other) /
                      metabolomics (Other) / mitochondria (Other) / one-carbon
                      flux (Other) / physiologic medium (Other) / reduced folate
                      carrier (Other) / serine hydroxymethyltransferase (Other)},
      cin          = {B070},
      ddc          = {570},
      cid          = {I:(DE-He78)B070-20160331},
      pnm          = {312 - Funktionelle und strukturelle Genomforschung
                      (POF4-312)},
      pid          = {G:(DE-HGF)POF4-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:33326752},
      doi          = {10.1016/j.cmet.2020.12.002},
      url          = {https://inrepo02.dkfz.de/record/166539},
}