ArticleThe Journal of investigative dermatology2013
Merkel cell polyomavirus-positive Merkel cell carcinoma cells do not require expression of the viral small T antigen.
Article in The Journal of investigative dermatology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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31 citing papers in PubMed, 67 citations in OpenAlex.
- Viral persistence and host-state remodeling in virus-associated cancers.Archives of microbiology · 2026Review
- An immunocompetent model of MCPyV-driven Merkel cell carcinoma reveals tumor evolution under immune selection.bioRxiv : the preprint server for biology · 2026Article
- MEK5/ERK5 inhibition sensitizes NRAS-mutant melanoma to MAPK-targeted therapy by preventing Cyclin D/CDK4-mediated G1/S progression.Cell death & disease · 2025Article
- Loss of p14 diminishes immunogenicity in melanoma via non-canonical Wnt signaling by reducing the peptide surface density.Molecular oncology · 2024Article
- Review
- Inhibition of p90 ribosomal S6 kinases disrupts melanoma cell growth and immune evasion.Journal of experimental & clinical cancer research : CR · 2023Article
- Onco-Pathogen Mediated Cancer Progression and Associated Signaling Pathways in Cancer Development.Pathogens (Basel, Switzerland) · 2023Review
- Merkel cell polyomavirus large T antigen binding to pRb promotes skin hyperplasia and tumor development.PLoS pathogens · 2022Article
- The Role of Histone Post-Translational Modifications in Merkel Cell Carcinoma.Frontiers in oncology · 2022Review
- Epigenetic Dysregulations in Merkel Cell Polyomavirus-Driven Merkel Cell Carcinoma.International journal of molecular sciences · 2021Review
- Role of Virus-Induced Host Cell Epigenetic Changes in Cancer.International journal of molecular sciences · 2021Review
- Article
- Article
- Merkel Cell Polyomavirus T Antigens Induce Merkel Cell-Like Differentiation in GLI1-Expressing Epithelial Cells.Cancers · 2020Article
- Merkel Cell Polyomavirus and Merkel Cell Carcinoma.Cancers · 2020Review
- CRISPR/Cas9 Editing of the Polyomavirus Tumor Antigens Inhibits Merkel Cell Carcinoma Growth In Vitro.Cancers · 2019Article
- Elucidating the mechanism of action of domatinostat (4SC-202) in cutaneous T cell lymphoma cells.Journal of hematology & oncology · 2019Article
- Histogenesis of Merkel Cell Carcinoma: A Comprehensive Review.Frontiers in oncology · 2019Review
- CCL17/TARC and CCR4 expression in Merkel cell carcinoma.Oncotarget · 2018Article
- Viral tumor antigen expression is no longer required in radiation-resistant subpopulation of JCV induced mouse medulloblastoma cells.Genes & cancer · 2018Article
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5 authors at 2 institutions in 2 countries.
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No grant is acknowledged in the PubMed record.
Abstract
Increasing evidence suggests that Merkel cell carcinoma (MCC) is caused by the Merkel cell polyomavirus (MCV). The viral sequence encodes for two potential oncoproteins, i.e., the small T antigen (sT) and the large T antigen (LT). Indeed, sT has recently been shown to bear transforming activity. Here, we confirm this observation by demonstrating focus formation upon expression of MCV sT in NIH3T3 fibroblasts. On the other hand, however, we provide evidence that established MCC cells do not require sT for growth and survival. Silencing of sT protein expression by two different sT-specific short hairpin RNAs (shRNAs) leads to variable degrees of growth retardation in MCV-positive MCC cell lines. However, these effects are not sT specific, as proliferation of MCV-negative cell lines is similarly affected by these sT shRNAs. Furthermore, ectopic expression of shRNA-insensitive sT does not revert the growth inhibition implicated by sT silencing. Finally, the unambiguous and specific growth inhibition induced by means of an shRNA targeting both T antigens, can be completely rescued by ectopic expression of LT alone, thus demonstrating a dispensable role of sT. Altogether, our results indicate that MCV LT is more relevant in maintaining the proliferation and survival of established MCC cell lines.
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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.