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@ARTICLE{Yang:182311,
      author       = {D. Yang$^*$ and T. D. Strobel$^*$ and J. Bulkescher$^*$ and
                      C. Tessmer$^*$ and I. Hofmann$^*$ and F. Hoppe-Seyler$^*$
                      and K. Hoppe-Seyler$^*$},
      title        = {{FAM}57{A} ({F}amily with {S}equence {S}imilarity 57
                      {M}ember {A}) {I}s a {C}ell-{D}ensity-{R}egulated {P}rotein
                      and {P}romotes the {P}roliferation and {M}igration of
                      {C}ervical {C}ancer {C}ells.},
      journal      = {Cells},
      volume       = {11},
      number       = {20},
      issn         = {2073-4409},
      address      = {Basel},
      publisher    = {MDPI},
      reportid     = {DKFZ-2022-02568},
      pages        = {3309},
      year         = {2022},
      note         = {#EA:F065#LA:F065#},
      abstract     = {The FAM57A (family with sequence similarity 57 member A)
                      gene is controversially discussed to possess pro- or
                      anti-tumorigenic potential. Here, we analyze the regulation
                      of cellular FAM57A protein levels and study the functional
                      role of FAM57A in HPV-positive cervical cancer cells. We
                      find that FAM57A protein expression strongly depends on cell
                      density, with FAM57A being readily detectable at low cell
                      density, but undetectable at high cell density. This
                      regulation occurs post-transcriptionally and is not mirrored
                      by corresponding changes at the RNA level. We further show
                      that FAM57A protein levels are highly increased in cervical
                      cancer cells cultivated at hypoxia compared to normoxia and
                      provide evidence that FAM57A is a hypoxia-responsive gene
                      under control of the α-subunit of the HIF-1
                      (hypoxia-inducible factor-1) transcription factor. Yet, the
                      strong relative increase of FAM57A protein levels in hypoxic
                      cells is predominantly cell-density-dependent and occurs
                      post-transcriptionally. Other anti-proliferative effectors
                      besides hypoxia, such as silencing of HPV E6/E7 oncogene
                      expression in cervical cancer cells, also result in an
                      increase of FAM57A levels compared to untreated cells.
                      Functional analyses reveal that FAM57A repression leads to
                      pronounced anti-proliferative as well as anti-migratory
                      effects in cervical cancer cells. Taken together, these
                      results provide insights into the regulation of FAM57A
                      protein levels and reveal that they underlie a tight
                      cell-density-dependent control. Moreover, they identify
                      FAM57A as a critical determinant for the phenotype of
                      cervical cancer cells, which promotes their proliferation
                      and migration capacities.},
      keywords     = {Humans / Female / Uterine Cervical Neoplasms: metabolism /
                      Oncogene Proteins, Viral: genetics / Oncogene Proteins,
                      Viral: metabolism / Papillomavirus E7 Proteins: genetics /
                      Papillomavirus E7 Proteins: metabolism / Papillomavirus
                      Infections / Repressor Proteins: genetics / Repressor
                      Proteins: metabolism / Transcription Factors / Cell
                      Proliferation / Hypoxia / Cell Count / RNA / FAM57A (Other)
                      / cervical cancer (Other) / human papillomavirus (HPV)
                      (Other) / hypoxia (Other) / Oncogene Proteins, Viral (NLM
                      Chemicals) / Papillomavirus E7 Proteins (NLM Chemicals) /
                      Repressor Proteins (NLM Chemicals) / Transcription Factors
                      (NLM Chemicals) / RNA (NLM Chemicals)},
      cin          = {F065 / W170},
      ddc          = {570},
      cid          = {I:(DE-He78)F065-20160331 / I:(DE-He78)W170-20160331},
      pnm          = {316 - Infektionen, Entzündung und Krebs (POF4-316)},
      pid          = {G:(DE-HGF)POF4-316},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:36291175},
      doi          = {10.3390/cells11203309},
      url          = {https://inrepo02.dkfz.de/record/182311},
}