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@ARTICLE{Berning:896717,
      author       = {Berning, Lena and Schlütermann, David and Friedrich,
                      Annabelle and Berleth, Niklas and Sun, Yadong and Wu,
                      Wenxian and Mendiburo, María José and Deitersen, Jana and
                      Brass, Hannah and Skowron, Margaretha A. and Hoffmann,
                      Michèle J. and Niegisch, Günter and Pietruszka, Jörg and
                      Stork, Björn},
      title        = {{P}rodigiosin {S}ensitizes {S}ensitive and {R}esistant
                      {U}rothelial {C}arcinoma {C}ells to {C}isplatin {T}reatment},
      journal      = {Molecules},
      volume       = {26},
      number       = {5},
      issn         = {1420-3049},
      address      = {Basel},
      publisher    = {MDPI},
      reportid     = {FZJ-2021-03550},
      pages        = {1294 -},
      year         = {2021},
      abstract     = {Cisplatin-based treatment is the standard of care therapy
                      for urothelial carcinomas. However, complex cisplatin
                      resistance mechanisms limit the success of this approach.
                      Both apoptosis and autophagy have been shown to contribute
                      to this resistance. Prodigiosin, a secondary metabolite from
                      various bacteria, exerts different biological activities
                      including the modulation of these two cellular stress
                      response pathways. We analyzed the effect of prodigiosin on
                      protein levels of different autophagy- and apoptosis-related
                      proteins in cisplatin-sensitive and -resistant urothelial
                      carcinoma cells (UCCs). Furthermore, we investigated the
                      effect on cell viability of prodigiosin alone or in
                      combination with cisplatin. We made use of four different
                      pairs of cisplatin-sensitive and -resistant UCCs. We found
                      that prodigiosin blocked autophagy in UCCs and re-sensitized
                      cisplatin-resistant cells to apoptotic cell death.
                      Furthermore, we found that prodigiosin is a potent
                      anticancer agent with nanomolar IC50 values in all tested
                      UCCs. In combination studies, we observed that prodigiosin
                      sensitized both cisplatin-sensitive and -resistant
                      urothelial carcinoma cell lines to cisplatin treatment with
                      synergistic effects in most tested cell lines. These effects
                      of prodigiosin are at least partially mediated by altering
                      lysosomal function, since we detected reduced activities of
                      cathepsin B and L. We propose that prodigiosin is a
                      promising candidate for the therapy of cisplatin-resistant
                      urothelial carcinomas, either as a single agent or in
                      combinatory therapeutic approaches},
      cin          = {IBOC / IBG-1},
      ddc          = {540},
      cid          = {I:(DE-Juel1)IBOC-20090406 / I:(DE-Juel1)IBG-1-20101118},
      pnm          = {2171 - Biological and environmental resources for
                      sustainable use (POF4-217)},
      pid          = {G:(DE-HGF)POF4-2171},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {33673611},
      UT           = {WOS:000628431800001},
      doi          = {10.3390/molecules26051294},
      url          = {https://juser.fz-juelich.de/record/896717},
}