ArticleCancers2020
Merkel Cell Polyomavirus T Antigens Induce Merkel Cell-Like Differentiation in GLI1-Expressing Epithelial Cells.
Article in Cancers, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 31 citations in OpenAlex.
- RB1 inactivation in cutaneous carcinomas.Histopathology · 2026Review
- Piwil-2 represents a poor prognosticator in Merkel cell carcinomas that regulates oncoproteins, cell cycle arrest and SOX-2 expression.Scientific reports · 2025Article
- The complex conundrum of Merkel cell carcinoma cellular ancestry.Cell death & disease · 2025Review
- EmergingFrontiers in cell and developmental biology · 2025Review
- Merkel Cell Polyomavirus T Antigen-Mediated Reprogramming in Adult Merkel Cell Progenitors.The Journal of investigative dermatology · 2023Article
- Review
- Investigation of the RB1-SOX2 axis constitutes a tool for viral status determination and diagnosis in Merkel cell carcinoma.Virchows Archiv : an international journal of pathology · 2022Article
- Merkel cell polyomavirus and associated Merkel cell carcinoma.Tumour virus research · 2022Review
- Merkel cell polyomavirus large T antigen binding to pRb promotes skin hyperplasia and tumor development.PLoS pathogens · 2022Article
- Evidence of an epithelial origin of Merkel cell carcinoma.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2022Article
- The Emerging Role of Hedgehog Signaling in Viral Infections.Frontiers in microbiology · 2022Review
- DNA-methylation patterns imply a common cellular origin of virus- and UV-associated Merkel cell carcinoma.Oncogene · 2022Article
- LRIG1 is a positive prognostic marker in Merkel cell carcinoma and Merkel cell carcinoma expresses epithelial stem cell markers.Virchows Archiv : an international journal of pathology · 2021Article
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- Article
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- From Merkel Cell Polyomavirus Infection to Merkel Cell Carcinoma Oncogenesis.Frontiers in microbiology · 2021Review
Corrections and comments
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Authors and funding
15 authors at 2 institutions in 2 countries.
Funding
Abstract
Merkel cell carcinoma (MCC) is an aggressive skin cancer frequently caused by the Merkel cell polyomavirus (MCPyV). It is still under discussion, in which cells viral integration and MCC development occurs. Recently, we demonstrated that a virus-positive MCC derived from a trichoblastoma, an epithelial neoplasia bearing Merkel cell (MC) differentiation potential. Accordingly, we hypothesized that MC progenitors may represent an origin of MCPyV-positive MCC. To sustain this hypothesis, phenotypic comparison of trichoblastomas and physiologic human MC progenitors was conducted revealing GLI family zinc finger 1 (GLI1), Keratin 17 (KRT 17), and SRY-box transcription factor 9 (SOX9) expressions in both subsets. Furthermore, GLI1 expression in keratinocytes induced transcription of the MC marker SOX2 supporting a role of GLI1 in human MC differentiation. To assess a possible contribution of the MCPyV T antigens (TA) to the development of an MC-like phenotype, human keratinocytes were transduced with TA. While this led only to induction of KRT8, an early MC marker, combined GLI1 and TA expression gave rise to a more advanced MC phenotype with SOX2, KRT8, and KRT20 expression. Finally, we demonstrated MCPyV-large T antigens' capacity to inhibit the degradation of the MC master regulator Atonal bHLH transcription factor 1 (ATOH1). In conclusion, our report suggests that MCPyV TA contribute to the acquisition of an MC-like phenotype in epithelial cells.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.