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@ARTICLE{Myacheva:182135,
      author       = {K. Myacheva$^*$ and A. Walsh and M. Riester$^*$ and G.
                      Pelos$^*$ and J. Carl$^*$ and S. Diederichs$^*$},
      title        = {{CRISPR}i screening identifies {CASP}8{AP}2 as an essential
                      viability factor in lung cancer controlling tumor cell death
                      via the {AP}-1 pathway.},
      journal      = {Cancer letters},
      volume       = {552},
      number       = {1},
      issn         = {0304-3835},
      address      = {Amsterdam [u.a.]},
      publisher    = {Elsevier Science},
      reportid     = {DKFZ-2022-02452},
      pages        = {215958},
      year         = {2023},
      note         = {#EA:B150#LA:B150# / 2023 Jan 1;552:215958},
      abstract     = {Since lung cancer remains the leading cause of cancer death
                      globally, there is an urgent demand for novel therapeutic
                      targets. We carried out a CRISPR interference (CRISPRi)
                      loss-of-function screen for human lung adenocarcinoma (LUAD)
                      targeting 2098 deregulated genes using a customized
                      algorithm to comprehensively probe the functionality of
                      every resolvable transcriptional start site (TSS). CASP8AP2
                      was identified as the only hit that significantly affected
                      the viability of all eight screened LUAD cell lines while
                      the viability of non-transformed lung cells was only
                      moderately impacted. Knockdown (KD) of CASP8AP2 induced both
                      autophagy and apoptotic cell death pathways. Systematic
                      expression profiling linked the AP-1 transcription factor to
                      the CASP8AP2 KD-induced cancer cell death. Furthermore,
                      inhibition of AP-1 reverted the CASP8AP2 silencing-induced
                      phenotype. Overall, the tailored CRISPRi screen profiled the
                      impact of over 2000 genes on the survival of eight LUAD cell
                      lines and identified the CASP8AP2 - AP-1 axis mediating lung
                      cancer viability.},
      keywords     = {Autophagy (Other) / CRISPR (Other) / Caspase (Other) /
                      FLASH (Other) / Lung adenocarcinoma (Other) / NSCLC (Other)},
      cin          = {B150 / FR01},
      ddc          = {570},
      cid          = {I:(DE-He78)B150-20160331 / I:(DE-He78)FR01-20160331},
      pnm          = {312 - Funktionelle und strukturelle Genomforschung
                      (POF4-312)},
      pid          = {G:(DE-HGF)POF4-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:36252816},
      doi          = {10.1016/j.canlet.2022.215958},
      url          = {https://inrepo02.dkfz.de/record/182135},
}