ArticleCell death & disease2019
SEPT9_i1 regulates human breast cancer cell motility through cytoskeletal and RhoA/FAK signaling pathway regulation.
Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
44 citing papers in PubMed, 73 citations in OpenAlex.
- High-Performance Prevascularized SHED-Laden rGO@Hydrogel Achieves Optimized Diabetic Bone Defect Repair.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Septins buffer actomyosin forces to protect the nucleus from genotoxic mechanical stress.bioRxiv : the preprint server for biology · 2026Article
- The Role of Actin-Binding Proteins in Breast Cancer Progression.Breast cancer (Dove Medical Press) · 2026Review
- Mechanical Signaling: Molecular Mechanisms, Biological Functions, Diseases, and Therapeutic Targets.MedComm · 2025Review
- 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
- Mechanosignaling and 3D morphological adaptation of MSCs in response to hydrogel rigidity underpin angiogenic and immunomodulatory efficacy for ischemic injury regeneration.Bioactive materials · 2025Article
- Application of Gene Editing Technology Based on Targeted Delivery Materials in TNBC.ACS omega · 2025Review
- LHPP-P38 MAPK/ERK-ETS1 Axis Negative Feedback Signaling Restrains Progression in Breast Cancer.Cancer science · 2025Article
- The immunoregulatory role of integrins in pulmonary diseases.Frontiers in immunology · 2025Review
- Mechanisms and therapeutic potential of disulphidptosis in cancer.Cell proliferation · 2025Review
- Dysregulation of septin cytoskeletal organization in the trabecular meshwork contributes to ocular hypertension.JCI insight · 2024Article
- Arginine methylation-dependent TRIM47 stability mediated by CARM1 promotes the metastasis of hepatocellular carcinoma.Cell death discovery · 2024Article
- SEPT9_i1 and Septin Dynamics in Oncogenesis and Cancer Treatment.Biomolecules · 2024Review
- Article
- METTL16 regulates the mRNA stability of FBXO5 via m6A modification to facilitate the malignant behavior of breast cancer.Cancer & metabolism · 2024Article
- The concerted action of SEPT9 and EPLIN modulates the adhesion and migration of human fibroblasts.Life science alliance · 2024Article
- Article
- Tuftelin1 drives experimental pulmonary fibrosis progression by facilitating stress fiber assembly.Respiratory research · 2023Article
- An oncogenic isoform of septin 9 promotes the formation of juxtanuclear invadopodia by reducing nuclear deformability.Cell reports · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Increasing cell mobility is the basis of tumor invasion and metastasis, and is therefore a therapeutic target for preventing the spread of many types of cancer. Septins are a family of cytoskeletal proteins with GTPase activity, and play a role in many important cellular functions, including cell migration. SEPT9 isoform 1 protein (SEPT9_i1) has been associated with breast tumor development and the enhancement of cell migration; however, the exact mechanism of how SEPT9_i1 might affect breast cancer progression remains to be elucidated. Here, we report that the expression of SEPT9_i1 positively correlated with paxillin, and both were significantly upregulated in invasive breast cancer tissues of patients with lymph node metastases. Lentivirus-mediated shRNA knockdown of SEPT9 in MCF-7 cells diminished tumor cell migration, focal adhesion (FA) maturation and the expression of β-actin, β-tubulin, Cdc42, RhoA, and Rac, whereas overexpression of SEPT9_i1 in SEPT9-knockdown MCF-7 cells promoted cell migration, FA maturation and relevant protein expression. Furthermore, overexpression of SEPT9_i1 in MCF-7 cells markedly increased FAK/Src/paxillin signaling, at least in part through RhoA/ROCK1 upstream activation. Transcriptome profiling suggested that SEPT9_i1 may directly affect "Focal adhesion" and "Regulation of actin cytoskeleton" signaling mechanisms. Finally, overexpression of SEPT9_i1 markedly enhanced lung metastases in vivo 6 weeks after tumor inoculation. These findings suggest that a mechanism of Septin-9-induced aberrant cancer cell migration is through cytoskeletal regulation and FA modulation, and encourages the use of SEPT9 as novel therapeutic target in the prevention of tumor metastasis.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.