@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{BrosinskyLeisterChengetal.2022,
  author    = {Brosinsky, Paulin and Leister, Hanna and Cheng, Nan and Varelas, Xaralabos and Visekruna, Alexander and Luu, Maik},
  title     = {Verteporfin protects against Th17 cell-mediated EAE independently of YAP inhibition},
  series = {European Journal of Immunology},
  volume    = {52},
  journal   = {European Journal of Immunology},
  number    = {9},
  doi       = {10.1002/eji.202149564},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-287234},
  pages     = {1523 -- 1526},
  year      = {2022},
  abstract  = {The known YAP inhibitor verteporfin is capable of repressing IL-17A production in Th17 cells. However, this effect is mediated independently of YAP and can ameliorate Th17-mediated experimental autoimmune encephalomyelitis (EAE) upon in vivo administration. The data suggest verteprofin's mode of action for the design of novel therapeutic autoimmune disease intervention.},
  language  = {en}
}