ArticleOncogene2019
Septin 9 isoforms promote tumorigenesis in mammary epithelial cells by increasing migration and ECM degradation through metalloproteinase secretion at focal adhesions.
Article in Oncogene, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 22 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
22 citing papers in PubMed, 38 citations in OpenAlex.
- Septins buffer actomyosin forces to protect the nucleus from genotoxic mechanical stress.bioRxiv : the preprint server for biology · 2026Article
- SEPT9 methylation as a diagnostic and predictive biomarker in the progression of ductal carcinoma in situ to invasive breast cancer.Scientific reports · 2025Article
- Single-cell mapping of alternative splicing linked to checkpoint immunotherapy response.Nucleic acids research · 2025Article
- Development and validation of a prognostic staging system for primary plasma cell leukemia.Journal of hematology & oncology · 2025Article
- Quantitative determination of the spatial distribution of components in single cells with CellDetail.Nature communications · 2024Article
- SEPT9_i1 and Septin Dynamics in Oncogenesis and Cancer Treatment.Biomolecules · 2024Review
- The concerted action of SEPT9 and EPLIN modulates the adhesion and migration of human fibroblasts.Life science alliance · 2024Article
- Dormant origin firing promotes head-on transcription-replication conflicts at transcription termination sites in response to BRCA2 deficiency.Nature communications · 2024Article
- An oncogenic isoform of septin 9 promotes the formation of juxtanuclear invadopodia by reducing nuclear deformability.Cell reports · 2023Article
- Septin11 promotes hepatocellular carcinoma cell motility by activating RhoA to regulate cytoskeleton and cell adhesion.Cell death & disease · 2023Article
- Septins as membrane influencers: direct play or in association with other cytoskeleton partners.Frontiers in cell and developmental biology · 2023Review
- Plasma-Methylated SEPT9 for the Noninvasive Diagnosis of Gastric Cancer.Journal of clinical medicine · 2022Article
- DCHS1, Lix1L, and the Septin Cytoskeleton: Molecular and Developmental Etiology of Mitral Valve Prolapse.Journal of cardiovascular development and disease · 2022Article
- Etodolac improves collagen induced rheumatoid arthritis in rats by inhibiting synovial inflammation, fibrosis and hyperplasia.Molecular biomedicine · 2021Article
- PIAS1 Regulates Hepatitis C Virus-Induced Lipid Droplet Accumulation by Controlling Septin 9 and Microtubule Filament Assembly.Pathogens (Basel, Switzerland) · 2021Article
- Proteomic profiling of the oncogenic septin 9 reveals isoform-specific interactions in breast cancer cells.Proteomics · 2021Article
- Cellular functions of actin- and microtubule-associated septins.Current biology : CB · 2021Review
- Reconstructed evolutionary history of the yeast septins Cdc11 and Shs1.G3 (Bethesda, Md.) · 2021Article
- The regulatory networks of the Hippo signaling pathway in cancer development.Journal of Cancer · 2021Review
- CDC42EP5/BORG3 modulates SEPT9 to promote actomyosin function, migration, and invasion.The Journal of cell biology · 2020Article
Corrections and comments
- Erratum issued
Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
Abstract
The cytoskeletal interacting protein Septin 9 (SEPT9), a member of the septin gene family, has been proposed to have oncogenic functions. It is a known hot spot of retroviral tagging insertion and a fusion partner of both de novo and therapy-induced mixed lineage leukemia (MLL). Of all septins, SEPT9 holds the strongest link to cancer, especially breast cancer. Murine models of breast cancer frequently exhibit SEPT9 amplification in the form of double minute chromosomes, and about 20% of human breast cancer display genomic amplification and protein over expression at the SEPT9 locus. Yet, a clear mechanism by which SEPT9 elicits tumor-promoting functions is lacking. To obtain unbiased insights on molecular signatures of SEPT9 upregulation in breast tumors, we overexpressed several of its isoforms in breast cancer cell lines. Global transcriptomic profiling supports a role of SEPT9 in invasion. Functional studies reveal that SEPT9 upregulation is sufficient to increase degradation of the extracellular matrix, while SEPT9 downregulation inhibits this process. The degradation pattern is peripheral and associated with focal adhesions (FAs), where it is coupled with increased expression of matrix metalloproteinases (MMPs). SEPT9 overexpression induces MMP upregulation in human tumors and in culture models and promotes MMP3 secretion to the media at FAs. Downregulation of SEPT9 or chemical inhibition of septin filament assembly impairs recruitment of MMP3 to FAs. Our results indicate that SEPT9 promotes upregulation and both trafficking and secretion of MMPs near FAs, thus enhancing migration and invasion of breast cancer cells.
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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.