ArticleOncogene2014
MMTV-Espl1 transgenic mice develop aneuploid, estrogen receptor alpha (ERα)-positive mammary adenocarcinomas.
Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 68 citations in OpenAlex.
- Separase activity distribution can be a marker of major molecular response and proliferation of CD34Annals of hematology · 2020Trial
- BRD4 regulates mActa pharmaceutica Sinica. B · 2025Article
- Bioinformatics insights intoFrontiers in cell and developmental biology · 2025Article
- PAX2 mediated upregulation of ESPL1 contributes to cisplatin resistance in bladder cancer through activating the JAK2/STAT3 pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Genome-wide CRISPR screen identifies ESPL1 limits the response of gastric cancer cells to apatinib.Cancer cell international · 2024Article
- Role of chromosomal cohesion and separation in aneuploidy and tumorigenesis.Cellular and molecular life sciences : CMLS · 2024Review
- Article
- Let-7c-5p Restrains Cell Growth and Induces Apoptosis of Lung Adenocarcinoma Cells via Targeting ESPL1.Molecular biotechnology · 2022Article
- Mapping separase-mediated cleavage in situ.NAR genomics and bioinformatics · 2022Article
- MicroRNA-202 safeguards meiotic progression by preventing premature SEPARASE-mediated REC8 cleavage.EMBO reports · 2022Article
- The CINSARC signature predicts the clinical outcome in patients with Luminal B breast cancer.NPJ breast cancer · 2021Article
- Article
- Aneuploidy as a promoter and suppressor of malignant growth.Nature reviews. Cancer · 2021Review
- ESPL1 Is a Novel Prognostic Biomarker Associated With the Malignant Features of Glioma.Frontiers in genetics · 2021Article
- Identification and analysis of genes associated with epithelial ovarian cancer by integrated bioinformatics methods.PloS one · 2021Article
- Structure and Function of the Separase-Securin Complex.Sub-cellular biochemistry · 2021Review
- p53 Is Not Required for High CIN to Induce Tumor Suppression.Molecular cancer research : MCR · 2021Article
- In vivo CRISPR/Cas9 knockout screen: TCEAL1 silencing enhances docetaxel efficacy in prostate cancer.Life science alliance · 2020Article
- The New Paradigm of Network Medicine to Analyze Breast Cancer Phenotypes.International journal of molecular sciences · 2020Article
- Centrosome reduction in newly-generated tetraploid cancer cells obtained by separase depletion.Scientific reports · 2020Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Separase, a protease encoded by the ESPL1 gene, cleaves the chromosomal cohesin during mitosis. Separase protein and transcripts are overexpressed in a wide range of human cancers. To investigate the physiological consequence of Separase overexpression in animals, we have generated a transgenic MMTV-Espl1 mouse model that overexpresses Separase protein in the mammary glands. MMTV-Espl1 mice in a C57BL/6 genetic background develop aggressive, highly aneuploid and estrogen receptor alpha-positive (ERα+) mammary adenocarcinomas with an 80% penetrance. The mammary tumors caused by overexpression of Separase, alone or combined with p53 heterozygosity, in mammary epithelium mimic several aspects of the most aggressive forms of human breast cancer, including high levels of genetic instability, cell cycle defects, poor differentiation, distant metastasis and metaplasia. Histopathologically, MMTV-Espl1 tumors are highly heterogeneous showing features of both luminal as well as basal subtypes of breast cancers, with aggressive disease phenotype. In addition to aneuploidy, Separase overexpression results in chromosomal instability (CIN) including premature chromatid separation (PCS), lagging chromosomes, anaphase bridges, micronuclei, centrosome amplification, multinucleated cells, gradual accumulation of DNA damage and progressive loss of tumor suppressors p53 and cadherin gene loci. These results suggest that Separase-overexpressing mammary cells are not only susceptible to chromosomal missegregation-induced aneuploidy but also other genetic instabilities including DNA damage and loss of key tumor suppressor gene loci, which in combination can initiate tumorigenesis and disease progression.
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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.