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@ARTICLE{Su:163946,
      author       = {Su, Yan and Huang, Hongyan and Luo, Tianzhi and Zheng, You
                      and Fan, Jie and Ren, He and Tang, Meng and Niu, Zubiao and
                      Wang, Chenxi and Wang, Yuqi and Zhang, Zhengrong and Liang,
                      Jianqing and Ruan, Banzhan and Gao, Lihua and Chen, Zhaolie
                      and Melino, Gerry and Wang, Xiaoning and Sun, Qiang},
      title        = {{C}ell-in-cell structure mediates in-cell killing
                      suppressed by {CD}44.},
      journal      = {Cell discovery},
      volume       = {8},
      number       = {1},
      issn         = {2056-5968},
      address      = {London},
      publisher    = {Nature Publishing Group},
      reportid     = {DZNE-2022-00620},
      pages        = {35},
      year         = {2022},
      abstract     = {Penetration of immune cells into tumor cells was believed
                      to be immune-suppressive via cell-in-cell (CIC) mediated
                      death of the internalized immune cells. We unexpectedly
                      found that CIC formation largely led to the death of the
                      host tumor cells, but not the internalized immune cells,
                      manifesting typical features of death executed by NK cells;
                      we named this 'in-cell killing' which displays the efficacy
                      superior to the canonical way of 'kiss-killing' from
                      outside. By profiling isogenic cells, CD44 on tumor cells
                      was identified as a negative regulator of 'in-cell killing'
                      via inhibiting CIC formation. CD44 functions to antagonize
                      NK cell internalization by reducing N-cadherin-mediated
                      intercellular adhesion and by enhancing Rho GTPase-regulated
                      cellular stiffness as well. Remarkably, antibody-mediated
                      blockade of CD44 signaling potentiated the suppressive
                      effects of NK cells on tumor growth associated with
                      increased heterotypic CIC formation. Together, we identified
                      CIC-mediated 'in-cell killing' as a promising strategy for
                      cancer immunotherapy.},
      cin          = {AG Nicotera},
      ddc          = {610},
      cid          = {I:(DE-2719)5000018},
      pnm          = {351 - Brain Function (POF4-351)},
      pid          = {G:(DE-HGF)POF4-351},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:35436988},
      pmc          = {pmc:PMC9016064},
      doi          = {10.1038/s41421-022-00387-1},
      url          = {https://pub.dzne.de/record/163946},
}