@article{FanZebischHornyetal.2020,
  author    = {Fan, Kaiji and Zebisch, Armin and Horny, Kai and Schrama, David and Becker, J{\"u}rgen C.},
  title     = {Highly expressed miR-375 is not an intracellular oncogene in Merkel cell polyomavirus-associated Merkel cell carcinoma},
  series = {Cancers},
  volume    = {12},
  journal   = {Cancers},
  number    = {3},
  issn      = {2072-6694},
  doi       = {10.3390/cancers12030529},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-200678},
  year      = {2020},
  abstract  = {miR-375 is a highly abundant miRNA in Merkel cell carcinoma (MCC). In other cancers, it acts as either a tumor suppressor or oncogene. While free-circulating miR-375 serves as a surrogate marker for tumor burden in patients with advanced MCC, its function within MCC cells has not been established. Nearly complete miR-375 knockdown in MCC cell lines was achieved using antagomiRs via nucleofection. The cell viability, growth characteristics, and morphology were not altered by this knockdown. miR-375 target genes and related signaling pathways were determined using Encyclopedia of RNA Interactomes (ENCORI) revealing Hippo signaling and epithelial to mesenchymal transition (EMT)-related genes likely to be regulated. Therefore, their expression was analyzed by multiplexed qRT-PCR after miR-375 knockdown, demonstrating only a limited change in expression. In summary, highly effective miR-375 knockdown in classical MCC cell lines did not significantly change the cell viability, morphology, or oncogenic signaling pathways. These observations render miR-375 an unlikely intracellular oncogene in MCC cells, thus suggesting that likely functions of miR-375 for the intercellular communication of MCC should be addressed.},
  language  = {en}
}
@article{RitterFanPaulsonetal.2016,
  author    = {Ritter, Cathrin and Fan, Kaiji and Paulson, Kelly G. and Nghiem, Paul and Schrama, David and Becker, J{\"u}rgen C.},
  title     = {Reversal of epigenetic silencing of MHC class I chain-related protein A and B improves immune recognition of Merkel cell carcinoma},
  series = {Scientific Reports},
  journal   = {Scientific Reports},
  number    = {21678},
  edition   = {6},
  doi       = {10.1038/srep21678},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-167992},
  year      = {2016},
  abstract  = {Merkel cell carcinoma (MCC) is a virally associated cancer characterized by its aggressive behavior and strong immunogenicity. Both viral infection and malignant transformation induce expression of MHC class I chain-related protein (MIC) A and B, which signal stress to cells of the immune system via Natural Killer group 2D (NKG2D) resulting in elimination of target cells. However, despite transformation and the continued presence of virally-encoded proteins, MICs are only expressed in a minority of MCC tumors in situ and are completely absent on MCC cell lines in vitro. This lack of MIC expression was due to epigenetic silencing via MIC promoter hypo-acetylation; indeed, MIC expression was re-induced by pharmacological inhibition of histone deacetylases (HDACs) both in vitro and in vivo. This re-induction of MICs rendered MCC cells more sensitive to immune-mediated lysis. Thus, epigenetic silencing of MICs is an important immune escape mechanism of MCCs.},
  language  = {en}
}