ArticleMolecular and cellular biology2015
Aurora B Overexpression Causes Aneuploidy and p21Cip1 Repression during Tumor Development.
Article in Molecular and cellular biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.
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Who cites it
73 citing papers in PubMed, 114 citations in OpenAlex.
- Epigenetic Factor Dysregulation and Distinct Expression Signatures in Retinoblastoma: A Transcriptomic Analysis.Investigative ophthalmology & visual science · 2026Article
- The Landscape of BRCA1-Associated Post-Translational Modifications.Cell biology international · 2026Review
- Cell line-dependent effects of β‑estradiol and testosterone on aurora kinases, GATA3, and associated miRNAs in hepatocellular carcinoma models HepG2 and Huh‑7.Cancer cell international · 2026Article
- RB dependent transcriptional regulation at mitotic centromeres preserves genome stability.Life science alliance · 2026Article
- AURKB-driven dissolution of CIZ1-RNA assemblies from the inactive X chromosome in mitosis.Nucleic acids research · 2026Article
- SPC24 boosts tumor progression and correlates with immune infiltrates in pancreatic adenocarcinoma.Frontiers in oncology · 2026Article
- Aurora kinase B as a therapeutic target in HPV-induced cervical cancer: mechanisms and future perspectives.Frontiers in oncology · 2026Review
- Ubiquitin specific protease 7 deubiquitinates and regulates Aurora B-mediated cytokinesis.BMB reports · 2025Article
- The multitalented TIP60 chromatin remodeling complex: wearing many hats in epigenetic regulation, cell division and diseases.Epigenetics & chromatin · 2025Review
- Targeting CDKs in cancer therapy: advances in PROTACs and molecular glues.NPJ precision oncology · 2025Review
- Aurora B and INCENP co-overexpression severely disrupts mitosis and distinctly modifies the global transcriptional landscape.iScience · 2025Article
- Transcriptome Analysis of Canine Histiocytic Sarcoma Tumors and Cell Lines Reveals Multiple Targets for Therapy.Cancers · 2025Article
- Mechanisms ofAmerican journal of translational research · 2025Article
- [High expression of AURKB promotes malignant phenotype of osteosarcoma cells by activating nuclear factor-κB signalingNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024Article
- Article
- Roles of ubiquitin‑specific protease 13 in normal physiology and tumors (Review).Oncology letters · 2024Review
- Identifying possible hub genes and biological mechanisms shared between bladder cancer and inflammatory bowel disease using machine learning and integrated bioinformatics.Journal of cancer research and clinical oncology · 2023Article
- Combination Therapy as a Promising Way to Fight Oral Cancer.Pharmaceutics · 2023Review
- Identification, characterization, and prognosis investigation of pivotal genes shared in different stages of breast cancer.Scientific reports · 2023Article
- Article
13 more citing papers are in PubMed but not listed here.
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
Abstract
Aurora kinase B, one of the three members of the mammalian Aurora kinase family, is the catalytic component of the chromosomal passenger complex, an essential regulator of chromosome segregation in mitosis. Aurora B is overexpressed in human tumors although whether this kinase may function as an oncogene in vivo is not established. Here, we report a new mouse model in which expression of the endogenous Aurkb locus can be induced in vitro and in vivo. Overexpression of Aurora B in cultured cells induces defective chromosome segregation and aneuploidy. Long-term overexpression of Aurora B in vivo results in aneuploidy and the development of multiple spontaneous tumors in adult mice, including a high incidence of lymphomas. Overexpression of Aurora B also results in a reduced DNA damage response and decreased levels of the p53 target p21(Cip1) in vitro and in vivo, in line with an inverse correlation between Aurora B and p21(Cip1) expression in human leukemias. Thus, overexpression of Aurora B may contribute to tumor formation not only by inducing chromosomal instability but also by suppressing the function of the cell cycle inhibitor p21(Cip1).
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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.