ArticleMolecular cancer research : MCR2014
NEDD9 regulates actin dynamics through cortactin deacetylation in an AURKA/HDAC6-dependent manner.
Article in Molecular cancer research : MCR, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 44 citations in OpenAlex.
- KDAC6 alters cell morphology and motility through positive and negative modulation of F-actin distribution.FEBS open bio · 2026Article
- Prevalence and Functional Roles of Intrinsic Disorder in the [F-actin]-monooxygenase MICAL Family Members and their Interactors.Cell biochemistry and biophysics · 2026Article
- Therapeutic potential of HDAC6 inhibitor Tubastatin A in health and diseases: current perspective and future directions.Military Medical Research · 2026Review
- Hic-5 drives epithelial mechanotransduction promoting a feed-forward cycle of bronchoconstriction.Nature communications · 2025Article
- Lysine deacetylase inhibitors have low selectivity in cells and exhibit predominantly off-target effects.FEBS open bio · 2025Article
- Inhibition of histone deacetylases attenuates tumor progression and improves immunotherapy in breast cancer.Frontiers in immunology · 2023Review
- HAT- and HDAC-Targeted Protein Acetylation in the Occurrence and Treatment of Epilepsy.Biomedicines · 2022Review
- In Silico Identification of lncRNAs Regulating Sperm Motility in the Turkey (International journal of molecular sciences · 2022Article
- Article
- Modulation of cellular processes by histone and non-histone protein acetylation.Nature reviews. Molecular cell biology · 2022Review
- Fe65: A Scaffolding Protein of Actin Regulators.Cells · 2021Review
- Critical review of non-histone human substrates of metal-dependent lysine deacetylases.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Review
- Cortactin function in invadopodia.Small GTPases · 2020Review
- KIF14 controls ciliogenesis via regulation of Aurora A and is important for Hedgehog signaling.The Journal of cell biology · 2020Article
- Review
- Emerging roles of histone modifications and HDACs in RNA splicing.Nucleic acids research · 2019Review
- Dual Targeting of Mesenchymal and Amoeboid Motility Hinders Metastatic Behavior.Molecular cancer research : MCR · 2017Article
- Combination of Eribulin and Aurora A Inhibitor MLN8237 Prevents Metastatic Colonization and Induces Cytotoxic Autophagy in Breast Cancer.Molecular cancer therapeutics · 2016Article
- Alisertib, an Aurora kinase A inhibitor, induces apoptosis and autophagy but inhibits epithelial to mesenchymal transition in human epithelial ovarian cancer cells.Drug design, development and therapy · 2015Article
- CAS proteins in health and disease: an update.IUBMB life · 2014Review
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10 authors at 1 institution in 1 country.
Funding
Abstract
unlabelledThe prometastatic protein NEDD9 (neural precursor cell expressed, developmentally downregulated 9) is highly expressed in many cancers and is required for mesenchymal individual cell migration and progression to the invasive stage. Nevertheless, the molecular mechanisms of NEDD9-driven migration and the downstream targets effecting metastasis are not well defined. In the current study, knockdown of NEDD9 in highly metastatic tumor cells drastically reduces their migratory capacity due to disruption of actin dynamics at the leading edge. Specifically, NEDD9 deficiency leads to a decrease in the persistence and stability of lamellipodial protrusions similar to knockdown of cortactin (CTTN). Mechanistically, it was shown that NEDD9 binds to and regulates acetylation of CTTN in an Aurora A kinase (AURKA)/HDAC6-dependent manner. The knockdown of NEDD9 or AURKA results in an increase in the amount of acetylated CTTN and a decrease in the binding of CTTN to F-actin. Overexpression of the deacetylation mimicking (9KR) mutant of CTTN is sufficient to restore actin dynamics at the leading edge and migration proficiency of the tumor cells. Inhibition of AURKA and HDAC6 activity by alisertib and Tubastatin A in xenograft models of breast cancer leads to a decrease in the number of pulmonary metastases. Collectively, these findings identify CTTN as the key downstream component of NEDD9-driven migration and metastatic phenotypes. IMPLICATIONS: This study provides a mechanistic platform for therapeutic interventions based on AURKA and HDAC6 inhibition for patients with metastatic breast cancer to prevent and/or eradicate metastases.
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