Cep55 overexpression promotes genomic instability and tumorigenesis in mice.
Animals
Biomarkers, Tumor
Biopsy
Cell Cycle Proteins
/ genetics
Cell Line
Cell Transformation, Neoplastic
/ genetics
Checkpoint Kinase 1
/ metabolism
Disease Susceptibility
Fibroblasts
/ metabolism
Gene Expression
Genomic Instability
Genotype
Immunohistochemistry
Karyotype
Lymph Nodes
/ metabolism
Mice
Mice, Transgenic
Microtubules
/ metabolism
Mitosis
Protein Stability
Proto-Oncogene Proteins c-akt
/ genetics
Signal Transduction
Stress, Physiological
Tumor Suppressor Protein p53
/ genetics
Journal
Communications biology
ISSN: 2399-3642
Titre abrégé: Commun Biol
Pays: England
ID NLM: 101719179
Informations de publication
Date de publication:
21 10 2020
21 10 2020
Historique:
received:
18
09
2019
accepted:
17
09
2020
entrez:
22
10
2020
pubmed:
23
10
2020
medline:
22
6
2021
Statut:
epublish
Résumé
High expression of centrosomal protein CEP55 has been correlated with clinico-pathological parameters across multiple human cancers. Despite significant in vitro studies and association of aberrantly overexpressed CEP55 with worse prognosis, its causal role in vivo tumorigenesis remains elusive. Here, using a ubiquitously overexpressing transgenic mouse model, we show that Cep55 overexpression causes spontaneous tumorigenesis and accelerates Trp53
Identifiants
pubmed: 33087841
doi: 10.1038/s42003-020-01304-6
pii: 10.1038/s42003-020-01304-6
pmc: PMC7578791
doi:
Substances chimiques
Biomarkers, Tumor
0
Cell Cycle Proteins
0
Cep55 protein, mouse
0
Trp53 protein, mouse
0
Tumor Suppressor Protein p53
0
Checkpoint Kinase 1
EC 2.7.11.1
Chek1 protein, mouse
EC 2.7.11.1
Proto-Oncogene Proteins c-akt
EC 2.7.11.1
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
593Références
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