TY  - JOUR
A1  - Fan, Kaiji
A1  - Zebisch, Armin
A1  - Horny, Kai
A1  - Schrama, David
A1  - Becker, Jürgen C.
T1  - Highly expressed miR-375 is not an intracellular oncogene in Merkel cell polyomavirus-associated Merkel cell carcinoma
JF  - Cancers
N2  - 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.
KW  - miR-375
KW  - antagomiRs
KW  - Merkel cell carcinoma
KW  - Hippo signaling
KW  - focal adhesion
Y1  - 2020
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-200678
SN  - 2072-6694
VL  - 12
IS  - 3
ER  - 
TY  - JOUR
A1  - Brosinsky, Paulin
A1  - Leister, Hanna
A1  - Cheng, Nan
A1  - Varelas, Xaralabos
A1  - Visekruna, Alexander
A1  - Luu, Maik
T1  - Verteporfin protects against Th17 cell‐mediated EAE independently of YAP inhibition
JF  - European Journal of Immunology
N2  - 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.
KW  - Hippo signaling
KW  - YAP
KW  - verteporfin
KW  - Th17 cells
KW  - EAE
Y1  - 2022
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-287234
VL  - 52
IS  - 9
SP  - 1523
EP  - 1526
ER  -