ArticleOncotarget2013
Genomic imbalance of HMMR/RHAMM regulates the sensitivity and response of malignant peripheral nerve sheath tumour cells to aurora kinase inhibition.
Article in Oncotarget, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
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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
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.
- Current status and recommendations for biomarkers and biobanking in neurofibromatosis.Neurology · 2016Guideline
- CD168 Identifies Proliferating Pancreatic Islet Cells in Murine and Human.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Expanding a precision medicine platform for malignant peripheral nerve sheath tumors: New patient-derived orthotopic xenografts, cell lines and tumor entities.Molecular oncology · 2024Article
- Article
- The role of RHAMM in cancer: Exposing novel therapeutic vulnerabilities.Frontiers in oncology · 2022Review
- From Genes to -Omics: The Evolving Molecular Landscape of Malignant Peripheral Nerve Sheath Tumor.Genes · 2020Review
- Article
- Aurora A kinase and its activator TPX2 are potential therapeutic targets in KRAS-induced pancreatic cancer.Cellular oncology (Dordrecht, Netherlands) · 2020Article
- The therapeutic potential of Aurora kinases targeting in glioblastoma: from preclinical research to translational oncology.Journal of molecular medicine (Berlin, Germany) · 2020Review
- Review
- Oleate acid-stimulated HMMR expression by CEBPα is associated with nonalcoholic steatohepatitis and hepatocellular carcinoma.International journal of biological sciences · 2020Article
- Cell activity during peripheral nerve defect repair process using a nerve scaffold.Oncotarget · 2017Article
- BRCA1 controls the cell division axis and governs ploidy and phenotype in human mammary cells.Oncotarget · 2017Article
- Aurora A kinase inhibition enhances oncolytic herpes virotherapy through cytotoxic synergy and innate cellular immune modulation.Oncotarget · 2017Article
- Carcinoma Cell Hyaluronan as a "Portable" Cancerized Prometastatic Microenvironment.Cancer research · 2016Review
- Article
- Interactions between Hyaluronan and Its Receptors (CD44, RHAMM) Regulate the Activities of Inflammation and Cancer.Frontiers in immunology · 2015Review
- Role of receptor for hyaluronan-mediated motility (RHAMM) in human head and neck cancers.Journal of cancer research and clinical oncology · 2014Review
- The Aurora-A inhibitor MLN8237 affects multiple mitotic processes and induces dose-dependent mitotic abnormalities and aneuploidy.Oncotarget · 2014Article
- Hyaluronan and RHAMM in wound repair and the "cancerization" of stromal tissues.BioMed research international · 2014Review
Corrections and comments
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Authors and funding
16 authors at 7 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Malignant peripheral nerve sheath tumours (MPNST) are rare, hereditary cancers associated with neurofibromatosis type I. MPNSTs lack effective treatment options as they often resist chemotherapies and have high rates of disease recurrence. Aurora kinase A (AURKA) is an emerging target in cancer and an aurora kinase inhibitor (AKI), termed MLN8237, shows promise against MPNST cell lines in vitro and in vivo. Here, we test MLN8237 against two primary human MPNST grown in vivo as xenotransplants and find that treatment results in tumour cells exiting the cell cycle and undergoing endoreduplication, which cumulates in stabilized disease. Targeted therapies can often fail in the clinic due to insufficient knowledge about factors that determine tumour susceptibilities, so we turned to three MPNST cell-lines to further study and modulate the cellular responses to AKI. We find that the sensitivity of cell-lines with amplification of AURKA depends upon the activity of the kinase, which correlates with the expression of the regulatory gene products TPX2 and HMMR/RHAMM. Silencing of HMMR/RHAMM, but not TPX2, augments AURKA activity and sensitizes MPNST cells to AKI. Furthermore, we find that AURKA activity is critical to the propagation and self-renewal of sphere-enriched MPNST cancer stem-like cells. AKI treatment significantly reduces the formation of spheroids, attenuates the self-renewal of spheroid forming cells, and promotes their differentiation. Moreover, silencing of HMMR/RHAMM is sufficient to endow MPNST cells with an ability to form and maintain sphere culture. Collectively, our data indicate that AURKA is a rationale therapeutic target for MPNST and tumour cell responses to AKI, which include differentiation, are modulated by the abundance of HMMR/RHAMM.
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