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@ARTICLE{Collura:307455,
author = {J. L. Collura and K. C. Lei$^*$ and M. Chandra and T.
Kervarrec and H. J. Park and M. Dalkoohi and J. Becker$^*$
and Y. Chang and P. S. Moore and M. Shuda},
title = {{P}harmacologic reversion of {M}erkel cell carcinoma via
{CBP}/p300 inhibition.},
journal = {Proceedings of the National Academy of Sciences of the
United States of America},
volume = {122},
number = {52},
issn = {0027-8424},
address = {Washington, DC},
publisher = {National Acad. of Sciences},
reportid = {DKFZ-2025-03054},
pages = {e2516667122},
year = {2025},
abstract = {Merkel cell polyomavirus (MCV) T antigen functions as an
oncoprotein that drives the transformation of Merkel cell
carcinoma (MCC) cells by activating transcription factors
involved in cell proliferation. The viral T antigen promoter
requires the activity of the cellular coactivator
CREB-binding protein (CBP)/p300 for its expression.
Inhibition of CBP/p300 with two distinct small-molecule
inhibitors suppresses T antigen expression, leading to cell
cycle arrest and upregulation of the cell cycle inhibitor
p27Kip1. This shift promotes neuronal differentiation,
associated with neurite outgrowth in MCC cells. RNA
sequencing revealed downregulation of genes involved in E2F,
Myc, mTORC1 oncogenic signaling, as well as markers of the
Merkel cell lineage including Sox2 and Atoh1. Notably, a
rare MCC case exhibiting a mixed cellular composition, with
loss of T antigen expression and neuroblastic phenotype,
showed a transcriptomic profile resembling that of MCC cells
treated with CBP/p300 inhibitors. This suggests that similar
differentiation processes may contribute to tumor
heterogeneity in patients. This study presents the model
system enabling reversible switching between a transformed
and differentiated cell state in a human cancer using
small-molecule treatment.},
keywords = {Carcinoma, Merkel Cell: drug therapy / Carcinoma, Merkel
Cell: metabolism / Carcinoma, Merkel Cell: pathology /
Carcinoma, Merkel Cell: genetics / Carcinoma, Merkel Cell:
virology / Humans / Merkel cell polyomavirus: metabolism /
E1A-Associated p300 Protein: antagonists $\&$ inhibitors /
E1A-Associated p300 Protein: metabolism / CREB-Binding
Protein: antagonists $\&$ inhibitors / CREB-Binding Protein:
metabolism / Cell Line, Tumor / Gene Expression Regulation,
Neoplastic: drug effects / Skin Neoplasms: drug therapy /
Skin Neoplasms: metabolism / Skin Neoplasms: pathology /
Skin Neoplasms: genetics / Antigens, Viral, Tumor:
metabolism / Antigens, Viral, Tumor: genetics / Cell
Proliferation: drug effects / Cell Differentiation: drug
effects / p300-CBP Transcription Factors: antagonists $\&$
inhibitors / p300-CBP Transcription Factors: metabolism /
CBP/p300 (Other) / Merkel cell carcinoma (Other) / Merkel
cell polyomavirus (Other) / T antigen (Other) / cancer
reversion (Other) / E1A-Associated p300 Protein (NLM
Chemicals) / CREB-Binding Protein (NLM Chemicals) / EP300
protein, human (NLM Chemicals) / CREBBP protein, human (NLM
Chemicals) / Antigens, Viral, Tumor (NLM Chemicals) /
p300-CBP Transcription Factors (NLM Chemicals)},
cin = {ED01},
ddc = {500},
cid = {I:(DE-He78)ED01-20160331},
pnm = {899 - ohne Topic (POF4-899)},
pid = {G:(DE-HGF)POF4-899},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:41439710},
doi = {10.1073/pnas.2516667122},
url = {https://inrepo02.dkfz.de/record/307455},
}