ArticleCell reports2023
An oncogenic isoform of septin 9 promotes the formation of juxtanuclear invadopodia by reducing nuclear deformability.
Article in Cell reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 7 citations in OpenAlex.
- Septins buffer actomyosin forces to protect the nucleus from genotoxic mechanical stress.The Journal of cell biology · 2026Article
- In Silico Identification of Conserved 'Fungal Islands' in Human Septin9: Evidence for Atavistic Therapeutic Targets.International journal of molecular sciences · 2026Article
- Septin crosstalk with microtubules and actin is regulated by a GSK3-dependent phosphoswitch.bioRxiv : the preprint server for biology · 2026Article
- Characterizing the salivary RNA landscape to identify potential diagnostic, prognostic, and follow-up biomarkers for breast cancer.Molecular oncology · 2026Article
- Septins buffer actomyosin forces to protect the nucleus from genotoxic mechanical stress.bioRxiv : the preprint server for biology · 2026Article
- Mechanically-induced Septin Networks Protect Nuclear Integrity.bioRxiv : the preprint server for biology · 2026Article
- Mechanical Signaling: Molecular Mechanisms, Biological Functions, Diseases, and Therapeutic Targets.MedComm · 2025Review
- Application of Gene Editing Technology Based on Targeted Delivery Materials in TNBC.ACS omega · 2025Review
- SEPT9_i1 and Septin Dynamics in Oncogenesis and Cancer Treatment.Biomolecules · 2024Review
- A Hierarchical Mechanotransduction System: From Macro to Micro.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Review
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Invadopodia are extracellular matrix (ECM) degrading structures, which promote cancer cell invasion. The nucleus is increasingly viewed as a mechanosensory organelle that determines migratory strategies. However, how the nucleus crosstalks with invadopodia is little known. Here, we report that the oncogenic septin 9 isoform 1 (SEPT9_i1) is a component of breast cancer invadopodia. SEPT9_i1 depletion diminishes invadopodium formation and the clustering of the invadopodium precursor components TKS5 and cortactin. This phenotype is characterized by deformed nuclei and nuclear envelopes with folds and grooves. We show that SEPT9_i1 localizes to the nuclear envelope and juxtanuclear invadopodia. Moreover, exogenous lamin A rescues nuclear morphology and juxtanuclear TKS5 clusters. Importantly, SEPT9_i1 is required for the amplification of juxtanuclear invadopodia, which is induced by the epidermal growth factor. We posit that nuclei of low deformability favor the formation of juxtanuclear invadopodia in a SEPT9_i1-dependent manner, which functions as a tunable mechanism for overcoming ECM impenetrability.
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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.