ArticleOncogene2016
The putative oncogene CEP72 inhibits the mitotic function of BRCA1 and induces chromosomal instability.
Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 30 citations in OpenAlex.
- Elevated CEP72 expression facilitates the progression of hepatocellular carcinoma and is associated with unfavorable outcomes.Discover oncology · 2025Article
- CCDC138 overexpression predicts poor prognosis and highlights ciliopathy-linked mechanisms in uterine corpus endometrial carcinoma.Frontiers in molecular biosciences · 2025Article
- An updated view on the centrosome as a cell cycle regulator.Cell division · 2022Review
- Loss of Cep72 affects the morphology of spermatozoa in mice.Frontiers in physiology · 2022Article
- The p53/p73 - p21Oncogene · 2021Article
- Mild replication stress causes aneuploidy by deregulating microtubule dynamics in mitosis.Cell cycle (Georgetown, Tex.) · 2019Article
- Ccdc61 controls centrosomal localization of Cep170 and is required for spindle assembly and symmetry.Molecular biology of the cell · 2018Article
- Noncoding RNA Ginir functions as an oncogene by associating with centrosomal proteins.PLoS biology · 2018Article
- Exploring the Role of Fallopian Ciliated Cells in the Pathogenesis of High-Grade Serous Ovarian Cancer.International journal of molecular sciences · 2018Review
- A New Linkage between the Tumor Suppressor RKIP and Autophagy: Targeted Therapeutics.Critical reviews in oncogenesis · 2018Review
- A systems medicine approach for finding target proteins affecting treatment outcomes in patients with non-Hodgkin lymphoma.PloS one · 2017Article
- CHK2-BRCA1 tumor-suppressor axis restrains oncogenic Aurora-A kinase to ensure proper mitotic microtubule assembly.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BRCA1 is a tumor-suppressor gene associated with, but not restricted to, breast and ovarian cancer and implicated in various biological functions. During mitosis, BRCA1 and its positive regulator Chk2 are localized at centrosomes and are required for the regulation of microtubule plus end assembly, thereby ensuring faithful mitosis and numerical chromosome stability. However, the function of BRCA1 during mitosis has not been defined mechanistically. To gain insights into the mitotic role of BRCA1 in regulating microtubule assembly, we systematically identified proteins interacting with BRCA1 during mitosis and found the centrosomal protein Cep72 as a novel BRCA1-interacting protein. CEP72 is frequently upregulated in colorectal cancer tissues and overexpression of CEP72 mirrors the consequences of BRCA1 loss during mitosis. In detail, the overexpression of CEP72 causes an increase in microtubule plus end assembly, abnormal mitotic spindle formation and the induction of chromosomal instability. Moreover, we show that high levels of Cep72 counteract Chk2 as a positive regulator of BRCA1 to ensure proper mitotic microtubule assembly. Thus, CEP72 represents a putative oncogene in colorectal cancer that might negatively regulate the mitotic function of BRCA1 to ensure chromosomal stability.
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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.