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@ARTICLE{Cheteh:125342,
      author       = {E. H. Cheteh and M. Augsten$^*$ and H. Rundqvist and J.
                      Bianchi and V. Sarne and L. Egevad and V. J. Bykov and A.
                      Östman and K. G. Wiman},
      title        = {{H}uman cancer-associated fibroblasts enhance glutathione
                      levels and antagonize drug-induced prostate cancer cell
                      death.},
      journal      = {Cell death $\&$ disease},
      volume       = {8},
      number       = {6},
      issn         = {2041-4889},
      address      = {London [u.a.]},
      publisher    = {Nature Publishing Group},
      reportid     = {DKFZ-2017-01475},
      pages        = {e2848 -},
      year         = {2017},
      abstract     = {Drug resistance is a major problem in cancer therapy. A
                      growing body of evidence demonstrates that the tumor
                      microenvironment, including cancer-associated fibroblasts
                      (CAFs), can modulate drug sensitivity in tumor cells. We
                      examined the effect of primary human CAFs on p53 induction
                      and cell viability in prostate cancer cells on treatment
                      with chemotherapeutic drugs. Co-culture with prostate CAFs
                      or CAF-conditioned medium attenuated DNA damage and the p53
                      response to chemotherapeutic drugs and enhanced prostate
                      cancer cell survival. CAF-conditioned medium inhibited the
                      accumulation of doxorubicin, but not taxol, in prostate
                      cancer cells in a manner that was associated with increased
                      cancer cell glutathione levels. A low molecular weight
                      fraction (<3 kDa) of CAF-conditioned medium had the same
                      effect. CAF-conditioned medium also inhibited induction of
                      reactive oxygen species (ROS) in both doxorubicin- and
                      taxol-treated cancer cells. Our findings suggest that CAFs
                      can enhance drug resistance in cancer cells by inhibiting
                      drug accumulation and counteracting drug-induced oxidative
                      stress. This protective mechanism may represent a novel
                      therapeutic target in cancer.},
      cin          = {A190},
      ddc          = {570},
      cid          = {I:(DE-He78)A190-20160331},
      pnm          = {311 - Signalling pathways, cell and tumor biology
                      (POF3-311)},
      pid          = {G:(DE-HGF)POF3-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:28569790},
      pmc          = {pmc:PMC5520886},
      doi          = {10.1038/cddis.2017.225},
      url          = {https://inrepo02.dkfz.de/record/125342},
}