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MCPyV Large T antigen induced atonal homolog 1 (ATOH1) is a lineage-dependency oncogene in Merkel cell carcinoma.

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https://hdl.handle.net/10037/17853
DOI
https://doi.org/10.1016/j.jid.2019.06.135
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Date
2019-07-07
Type
Journal article
Tidsskriftartikkel
Peer reviewed

Author
Fan, Kaiji; Gravemeyer, Jan; Ritter, Cathrin; Rasheed, Kashif; Gambichler, Thilo; Moens, Ugo Lionel; Shuda, Masahiro; Schrama, David; Becker, Jürgen C.
Abstract
Despite the fact that the transcription factor ATOH1 is a master regulator of Merkel cell development, its role in Merkel cell carcinoma (MCC) carcinogenesis remains controversial. Here, we provide several lines of evidence that ATOH1 is a lineage-dependent oncogene in MCC. Luciferase assays revealed binding of ATOH1 and subsequent activation to the promoter of miR-375, which is one of the most abundant microRNAs in MCCs. Overexpression of ATOH1 in variant MCC cell lines and fibroblasts induced miR-375 expression, whereas ATOH1 knockdown in classical MCC cell lines reduced miR-375 expression. Moreover, ATOH1 overexpression in these cells changed their growth characteristics from adherent to suspension and/orspheroidal growth, that is, resembling the neuroendocrine growth pattern of classical MCC cell lines. Notably, ectopic expression of different Merkel cell polyomavirus (MCPyV)-derived truncated large T antigens induced ATOH1 expression in fibroblasts, which was paralleled by miR-375 expression and similar morphologic changes. In summary, MCPyV-associated carcinogenesis is likely to induce the characteristic neuroendocrine features of MCC via induction of ATOH1; thus, ATOH1 can be regarded as a lineage-dependent oncogene in MCC.
Publisher
Elsevier
Citation
Fan, K.; Gravemeyer, J.,, Ritter, C., Rasheed, K.; Gambichler, T.; Moens,U.; Shuda, M.; Schrama, D.; Becker, J.C. (2019) MCPyV Large T antigen induced atonal homolog 1 (ATOH1) is a lineage-dependency oncogene in Merkel cell carcinoma. Journal of Investigative Dermatology, 2019
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  • Artikler, rapporter og annet (medisinsk biologi) [1103]
Copyright 2019 The Authors. Published by Elsevier, Inc. on behalf of the Society for Investigative Dermatology

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