ArticleMolecular cancer2014
The negative interplay between Aurora A/B and BRCA1/2 controls cancer cell growth and tumorigenesis via distinct regulation of cell cycle progression, cytokinesis, and tetraploidy.
Article in Molecular cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 32 citations in OpenAlex.
- Expanding Synthetic Lethality in DNA Damage Response-Defective Cancers Through Stress Phenotype-Guided Kinase Targeting.International journal of molecular sciences · 2026Review
- The Landscape of BRCA1-Associated Post-Translational Modifications.Cell biology international · 2026Review
- BRCA1 orchestrates the response to BI-2536 and its combination with alisertib in MYC-driven small cell lung cancer.Cell death & disease · 2024Article
- Cellular mechanisms mediating the anti-cancer effects of carnosol on gingiva carcinoma.Scientific reports · 2024Article
- AURKA promotes renal cell carcinoma progression via regulation of CCNB1 transcription.Heliyon · 2024Article
- AURKB Enhances Chromosomal Remodeling of Telomeric Genes and Accelerates Tumorigenesis of Uveal Melanoma.Investigative ophthalmology & visual science · 2023Article
- Article
- Aurora kinase A, a synthetic lethal target for precision cancer medicine.Experimental & molecular medicine · 2021Review
- Aurora Kinase B Inhibition: A Potential Therapeutic Strategy for Cancer.Molecules (Basel, Switzerland) · 2021Review
- Pterostilbene Sensitizes Cisplatin-Resistant Human Bladder Cancer Cells with OncogenicCancers · 2020Article
- Aurora kinases in ovarian cancer.ESMO open · 2020Review
- ID1 confers cancer cell chemoresistance through STAT3/ATF6-mediated induction of autophagy.Cell death & disease · 2020Article
- Mechanism of cytokinesis failure in ovarian cystadenomas with defective BRCA1 and P53 pathways.International journal of cancer · 2018Article
- Identifying genes as potential prognostic indicators in patients with serous ovarian cancer resistant to carboplatin using integrated bioinformatics analysis.Oncology reports · 2018Article
- AURKA inhibition mimics BRCAness.Aging · 2017Article
- Aurora A kinase regulates non-homologous end-joining and poly(ADP-ribose) polymerase function in ovarian carcinoma cells.Oncotarget · 2017Article
- Kinase signaling and targeted therapy for primary myelofibrosis.Experimental hematology · 2017Review
- The identification of a novel role for BRCA1 in regulating RNA polymerase I transcription.Oncotarget · 2016Article
- The long non-coding RNA ANRIL promotes proliferation and cell cycle progression and inhibits apoptosis and senescence in epithelial ovarian cancer.Oncotarget · 2016Article
- Bufalin enhances antitumor effect of paclitaxel on cervical tumorigenesis via inhibiting the integrin α2/β5/FAK signaling pathway.Oncotarget · 2016Article
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It is well known that the activation of Aurora A/B (Aur A/B) or inactivation of BRCA1/2 induces tumor formation. Others and we have reported that the mutual suppression between Aur A/B and BRCA1/2 may manipulate cancer cell growth and tumorigenesis, however, the interactive regulation and mechanism between these molecules are still elusive. In this study, by consecutive silencing of Aur A/B or/and BRCA1/2 with specific shRNAs, we showed that, in BRCA2-deficient pancreatic cancer cell line Capan-1 and in ovarian cancer cell line OVCA433, Aur A/B and BRCA1/2 inversely regulated the expression of each other likely through proteasome-mediated proteolysis but not through gene transcription. Aur A/B and BRCA1/2 conversely regulated cell cycle progression mainly through control of p53 and cyclin A. Moreover, the disruption of Aur A/B blocked abnormal cytokinesis and decreased cell multinuclearity and chromosome tetraploidy, whereas the deprivation of BRCA1/2 promoted the abnormal cytokinesis and enhanced the cell multinuclearity and tetraploidy. Furthermore, we showed by animal assays that the depletion of Aur A/B inhibited tumor growth of both cell lines, while the knockdown of BRCA1/2 promoted the tumor growth. However, the concurrent silencing of Aur A/B and BRCA1/2 diminished the effects of these molecules on the regulation of cell cycle, cytokinesis, and tetraploidy, leading to the burdened tumor sizes similar to those induced by scrambled shRNA-treated control cells. In summary, our study revealed that the negative interplay between Aur A/B and BRCA1/2 inversely controls the cell proliferation, cell cycle progression, cell multinuclearity, and tetraploidization to modulate tumorigenesis.
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