ArticleThe Journal of biological chemistry2012
Aurora B is regulated by the mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) signaling pathway and is a valuable potential target in melanoma cells.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
49 citing papers in PubMed, 76 citations in OpenAlex.
- FOXM1-associated melanoma stratification: integrated multi-omics and experimental validation reveal prognostic significance and therapeutic potential.BMC cancer · 2026Article
- Predicting condition-aware drug-induced transcriptional responses via a latent diffusion model.Bioinformatics (Oxford, England) · 2026Article
- Article
- Combined KRAS-MAPK pathway inhibitors and HER2-directed drug conjugate is efficacious in pancreatic cancer.Nature communications · 2024Article
- High In Vitro and In Vivo Activity of BI-847325, a Dual MEK/Aurora Kinase Inhibitor, in Human Solid and Hematologic Cancer Models.Cancer research communications · 2023Article
- Article
- The future of targeted kinase inhibitors in melanoma.Pharmacology & therapeutics · 2022Review
- High expression of aurora kinase B predicts poor prognosis in hepatocellular carcinoma after curative surgery and its effects on the tumor microenvironment.Annals of translational medicine · 2022Article
- Targeting senescence as an anticancer therapy.Molecular oncology · 2022Review
- Endogenous DOPA inhibits melanoma through suppression of CHRM1 signaling.Science advances · 2022Article
- CNOT3 interacts with the Aurora B and MAPK/ERK kinases to promote survival of differentiating mesendodermal progenitor cells.Molecular biology of the cell · 2021Article
- "Metalloestrogenic" effects of cadmium downstream of G protein-coupled estrogen receptor and mitogen-activated protein kinase pathways in human uterine fibroid cells.Archives of toxicology · 2021Article
- Adhesion-growth factor crosstalk regulates AURKB activation and ERK signalling in re-adherent fibroblasts.Journal of biosciences · 2021Article
- USP13 controls the stability of Aurora B impacting progression through the cell cycle.Oncogene · 2020Article
- Evolution of an Amniote-Specific Mechanism for Modulating Ubiquitin Signaling via Phosphoregulation of the E2 Enzyme UBE2D3.Molecular biology and evolution · 2020Article
- Co-regulation of the antagonistic RepoMan:Aurora-B pair in proliferating cells.Molecular biology of the cell · 2020Article
- Augmentation of danusertib's anticancer activity against melanoma by blockage of autophagy.Drug delivery and translational research · 2020Article
- HI-511 overcomes melanoma drug resistanceTheranostics · 2020Article
- FOXM1 and Cancer: Faulty Cellular Signaling Derails Homeostasis.Frontiers in oncology · 2020Review
- Identification of key genes involved in the pathogenesis of cutaneous melanoma using bioinformatics analysis.The Journal of international medical research · 2020Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Metastatic melanoma is a deadly skin cancer and is resistant to almost all existing treatment. Vemurafenib, which targets the BRAFV600E mutation, is one of the drugs that improves patient outcome, but the patients next develop secondary resistance and a return to cancer. Thus, new therapeutic strategies are needed to treat melanomas and to increase the duration of v-Raf murine sarcoma viral oncogene homolog B1 (BRAF) inhibitor response. The ERK pathway controls cell proliferation, and Aurora B plays a pivotal role in cell division. Here, we confirm that Aurora B is highly expressed in metastatic melanoma cells and that Aurora B inhibition triggers both senescence-like phenotypes and cell death in melanoma cells. Furthermore, we show that the BRAF/ERK axis controls Aurora B expression at the transcriptional level, likely through the transcription factor FOXM1. Our results provide insight into the mechanism of Aurora B regulation and the first molecular basis of Aurora B regulation in melanoma cells. The inhibition of Aurora B expression that we observed in vemurafenib-sensitive melanoma cells was rescued in cells resistant to this drug. Consistently, these latter cells remain sensitive to the effect of the Aurora B inhibitor. Noteworthy, wild-type BRAF melanoma cells are also sensitive to Aurora B inhibition. Collectively, our findings, showing that Aurora B is a potential target in melanoma cells, particularly in those vemurafenib-resistant, may open new avenues to improve the treatment of metastatic melanoma.
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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.