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@ARTICLE{MonfortVengut:298228,
      author       = {A. Monfort-Vengut and N. Sanz-Gómez and S.
                      Ballesteros-Sánchez and B. Ortigosa and A. Cambón and M.
                      Ramos$^*$ and Á. M. Lorenzo and M. Escribano-Cebrián and
                      J. M. Rosa-Rosa and J. Martínez-López and R.
                      Sánchez-Prieto and R. Sotillo$^*$ and G. de Cárcer},
      title        = {{O}smotic stress influences microtubule drug response via
                      {WNK}1 kinase signaling.},
      journal      = {Drug resistance updates},
      volume       = {79},
      issn         = {1368-7646},
      address      = {Oxford},
      publisher    = {Elsevier},
      reportid     = {DKFZ-2025-00235},
      pages        = {101203},
      year         = {2025},
      abstract     = {Ion homeostasis is critical for numerous cellular
                      processes, and disturbances in ionic balance underlie
                      diverse pathological conditions, including cancer
                      progression. Targeting ion homeostasis is even considered as
                      a strategy to treat cancer. However, very little is known
                      about how ion homeostasis may influence anticancer drug
                      response. In a genome-wide CRISPR-Cas9 resistance drug
                      screen, we identified and validated the master osmostress
                      regulator WNK1 kinase as a modulator of the response to the
                      mitotic inhibitor rigosertib. Osmotic stress and WNK1
                      inactivation lead to an altered response not only to
                      rigosertib treatment but also to other microtubule-related
                      drugs, minimizing the prototypical mitotic arrest produced
                      by these compounds. This effect is due to an alteration in
                      microtubule stability and polymerization dynamics, likely
                      maintained by fluctuations in intracellular molecular
                      crowding upon WNK1 inactivation. This promotes resistance to
                      microtubule depolymerizing compounds, and increased
                      sensitivity to microtubule stabilizing drugs. In summary,
                      our data proposes WNK1 osmoregulation activity as an
                      important modulator for microtubule-associated chemotherapy
                      response.},
      keywords     = {Microtubule dynamics (Other) / Mitosis (Other) / Osmotic
                      stress (Other) / Rigosertib (Other) / WNK1 (Other)},
      cin          = {B220},
      ddc          = {610},
      cid          = {I:(DE-He78)B220-20160331},
      pnm          = {312 - Funktionelle und strukturelle Genomforschung
                      (POF4-312)},
      pid          = {G:(DE-HGF)POF4-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:39855050},
      doi          = {10.1016/j.drup.2025.101203},
      url          = {https://inrepo02.dkfz.de/record/298228},
}