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@ARTICLE{Nisar:269344,
      author       = {Nisar, Hasan and Sanchidrián González, Paulina Mercedes
                      and Labonté, Frederik M and Schmitz, Claudia and Roggan,
                      Marie Denise and Kronenberg, Jessica and Konda, Bikash and
                      Chevalier, François and Hellweg, Christine E},
      title        = {{NF}-κ{B} in the {R}adiation {R}esponse of {A}549
                      {N}on-{S}mall {C}ell {L}ung {C}ancer {C}ells to {X}-rays and
                      {C}arbon {I}ons under {H}ypoxia.},
      journal      = {International journal of molecular sciences},
      volume       = {25},
      number       = {8},
      issn         = {1422-0067},
      address      = {Basel},
      publisher    = {Molecular Diversity Preservation International},
      reportid     = {DZNE-2024-00513},
      pages        = {4495},
      year         = {2024},
      abstract     = {Cellular hypoxia, detectable in up to $80\%$ of non-small
                      cell lung carcinoma (NSCLC) tumors, is a known cause of
                      radioresistance. High linear energy transfer (LET) particle
                      radiation might be effective in the treatment of hypoxic
                      solid tumors, including NSCLC. Cellular hypoxia can activate
                      nuclear factor κB (NF-κB), which can modulate
                      radioresistance by influencing cancer cell survival. The
                      effect of high-LET radiation on NF-κB activation in hypoxic
                      NSCLC cells is unclear. Therefore, we compared the effect of
                      low (X-rays)- and high (12C)-LET radiation on NF-κB
                      responsive genes' upregulation, as well as its target
                      cytokines' synthesis in normoxic and hypoxic A549 NSCLC
                      cells. The cells were incubated under normoxia $(20\%$ O2)
                      or hypoxia $(1\%$ O2) for 48 h, followed by irradiation with
                      8 Gy X-rays or 12C ions, maintaining the oxygen conditions
                      until fixation or lysis. Regulation of NF-κB responsive
                      genes was evaluated by mRNA sequencing. Secretion of NF-κB
                      target cytokines, IL-6 and IL-8, was quantified by ELISA. A
                      greater fold change increase in expression of NF-κB target
                      genes in A549 cells following exposure to 12C ions compared
                      to X-rays was observed, regardless of oxygenation status.
                      These genes regulate cell migration, cell cycle, and cell
                      survival. A greater number of NF-κB target genes was
                      activated under hypoxia, regardless of irradiation status.
                      These genes regulate cell migration, survival,
                      proliferation, and inflammation. X-ray exposure under
                      hypoxia additionally upregulated NF-κB target genes
                      modulating immunosurveillance and epithelial-mesenchymal
                      transition (EMT). Increased IL-6 and IL-8 secretion under
                      hypoxia confirmed NF-κB-mediated expression of
                      pro-inflammatory genes. Therefore, radiotherapy,
                      particularly with X-rays, may increase tumor invasiveness in
                      surviving hypoxic A549 cells.},
      keywords     = {Humans / NF-kappa B: metabolism / A549 Cells / Carcinoma,
                      Non-Small-Cell Lung: metabolism / Carcinoma, Non-Small-Cell
                      Lung: radiotherapy / Carcinoma, Non-Small-Cell Lung:
                      pathology / Carcinoma, Non-Small-Cell Lung: genetics / Lung
                      Neoplasms: metabolism / Lung Neoplasms: radiotherapy / Lung
                      Neoplasms: pathology / Lung Neoplasms: genetics / X-Rays /
                      Gene Expression Regulation, Neoplastic: radiation effects /
                      Linear Energy Transfer / Cell Hypoxia: radiation effects /
                      Carbon / Cell Survival: radiation effects / Radiation
                      Tolerance / Interleukin-8: metabolism / Interleukin-8:
                      genetics / NF-κB (Other) / 12C ions (Other) / A549 (Other)
                      / IL-6/IL-8 secretion (Other) / NF-κB (Other) / high-LET
                      radiation (Other) / hypoxia-induced radioresistance (Other)
                      / p65 (RelA) nuclear localization (Other) / tumor hypoxia
                      (Other) / NF-kappa B (NLM Chemicals) / Carbon (NLM
                      Chemicals) / Interleukin-8 (NLM Chemicals)},
      cin          = {AG Fuhrmann},
      ddc          = {540},
      cid          = {I:(DE-2719)1011004},
      pnm          = {352 - Disease Mechanisms (POF4-352)},
      pid          = {G:(DE-HGF)POF4-352},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:38674080},
      pmc          = {pmc:PMC11050661},
      doi          = {10.3390/ijms25084495},
      url          = {https://pub.dzne.de/record/269344},
}