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@ARTICLE{Ramesh:299486,
      author       = {P. Ramesh and A. R. Al Kadi and G. M. Borse and M.
                      Webendörfer and G. Zaun and M. Metzenmacher and F. Doerr
                      and S. Bölükbas and B. Hegedüs and S. S. Lueong$^*$ and
                      J. Magne and B. Liu and G. Nunez and M. Schuler and D. R.
                      Green and H. Kalkavan$^*$},
      title        = {{BCL}-{B} {P}romotes {L}ung {C}ancer {I}nvasiveness by
                      {D}irect {I}nhibition of {BOK}.},
      journal      = {Cells},
      volume       = {14},
      number       = {4},
      issn         = {2073-4409},
      address      = {Basel},
      publisher    = {MDPI},
      reportid     = {DKFZ-2025-00446},
      pages        = {246},
      year         = {2025},
      abstract     = {Expression of BCL-B, an anti-apoptotic BCL-2 family member,
                      is correlated with worse survival in lung adenocarcinomas.
                      Here, we show that BCL-B can mitigate cell death initiation
                      through interaction with the effector protein BOK. We found
                      that this interaction can promote sublethal mitochondrial
                      outer membrane permeabilization (MOMP) and consequently
                      generate apoptosis-flatliners, which represent a source of
                      drug-tolerant persister cells (DTPs). The engagement of
                      endothelial-mesenchymal-transition (EMT) further promotes
                      cancer cell invasiveness in such DTPs. Our results reveal
                      that BCL-B fosters cancer cell aggressiveness by
                      counteracting complete MOMP.},
      keywords     = {Humans / Lung Neoplasms: pathology / Lung Neoplasms:
                      metabolism / Lung Neoplasms: genetics / Neoplasm
                      Invasiveness / Proto-Oncogene Proteins c-bcl-2: metabolism /
                      Apoptosis / Cell Line, Tumor / Epithelial-Mesenchymal
                      Transition: genetics / Mitochondrial Membranes: metabolism /
                      BCL-2 family (Other) / BCL-B (Other) / BOK (Other) / DTP
                      (Other) / EMT (Other) / cancer (Other) / drug-resistance
                      (Other) / invasiveness (Other) / mitochondrial
                      permeabilization (Other) / persister phenotype (Other) /
                      Proto-Oncogene Proteins c-bcl-2 (NLM Chemicals)},
      cin          = {ED01},
      ddc          = {570},
      cid          = {I:(DE-He78)ED01-20160331},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:39996719},
      pmc          = {pmc:PMC11853756},
      doi          = {10.3390/cells14040246},
      url          = {https://inrepo02.dkfz.de/record/299486},
}