ArticleOncotarget2016
MDA-9/Syntenin (SDCBP) modulates small GTPases RhoA and Cdc42 via transforming growth factor β1 to enhance epithelial-mesenchymal transition in breast cancer.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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
33 citing papers in PubMed, 47 citations in OpenAlex.
- Targeting MDA-9/syntenin-1 (SDCBP) as a strategy to eliminate head and neck squamous cell carcinoma stem cells.Cancer letters · 2026Article
- Article
- The Role of Actin-Binding Proteins in Breast Cancer Progression.Breast cancer (Dove Medical Press) · 2026Review
- Implications of Altered Endosomal-Lysosomal Biogenesis in Melanoma Pathogenesis.International journal of molecular sciences · 2025Review
- MDA-9/Syntenin as a therapeutic cancer metastasis target: current molecular and preclinical understanding.Expert opinion on therapeutic targets · 2025Review
- Proteomic insights into breast cancer response to brain cell-secreted factors.Scientific reports · 2024Article
- Dexrazoxane inhibits the growth of esophageal squamous cell carcinoma by attenuating SDCBP/MDA-9/syntenin-mediated EGFR-PI3K-Akt pathway activation.Scientific reports · 2024Article
- Actionable spontaneous antibody responses antagonize malignant progression in ovarian carcinoma.Gynecologic oncology · 2023Article
- The Multifunctional Protein Syntenin-1: Regulator of Exosome Biogenesis, Cellular Function, and Tumor Progression.International journal of molecular sciences · 2023Review
- Biological Role and Aberrant Overexpression of Syntenin-1 in Cancer: Potential Role as a Biomarker and Therapeutic Target.Biomedicines · 2023Review
- Inhibitors against Two PDZ Domains of MDA-9 Suppressed Migration of Breast Cancer Cells.International journal of molecular sciences · 2023Article
- Peptide-Based Vaccines in Clinical Phases and New Potential Therapeutic Targets as a New Approach for Breast Cancer: A Review.Vaccines · 2022Review
- A Novel Necroptosis-Associated lncRNA Signature Can Impact the Immune Status and Predict the Outcome of Breast Cancer.Journal of immunology research · 2022Article
- Syntenin Regulated by miR-216b Promotes Cancer Progression in Pancreatic Cancer.Frontiers in oncology · 2022Article
- Targeting PDZ domains as potential treatment for viral infections, neurodegeneration and cancer.Biology direct · 2021Review
- SDCBP Modulates Stemness and Chemoresistance in Head and Neck Squamous Cell Carcinoma through Src Activation.Cancers · 2021Article
- Pharmacological inhibition of MDA-9/Syntenin blocks breast cancer metastasis through suppression of IL-1β.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Temporal multiomic modeling reveals a B-cell receptor proliferative program in chronic lymphocytic leukemia.Leukemia · 2021Article
- Role and clinical significance of TGF‑β1 and TGF‑βR1 in malignant tumors (Review).International journal of molecular medicine · 2021Review
- Prune-1 drives polarization of tumor-associated macrophages (TAMs) within the lung metastatic niche in triple-negative breast cancer.iScience · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Epithelial-mesenchymal transition (EMT) is one of the decisive steps regulating cancer invasion and metastasis. However, the molecular mechanisms underlying this transition require further clarification. MDA-9/syntenin (SDCBP) expression is elevated in breast cancer patient samples as well as cultured breast cancer cells. Silencing expression of MDA-9 in mesenchymal metastatic breast cancer cells triggered a change in cell morphology in both 2D- and 3D-cultures to a more epithelial-like phenotype, along with changes in EMT markers, cytoskeletal rearrangement and decreased invasion. Conversely, over expressing MDA-9 in epithelial non-metastatic breast cancer cells instigated a change in morphology to a more mesenchymal phenotype with corresponding changes in EMT markers, cytoskeletal rearrangement and an increase in invasion. We also found that MDA-9 upregulated active levels of known modulators of EMT, the small GTPases RhoA and Cdc42, via TGFβ1. Reintroducing TGFβ1 in MDA-9 silenced cells restored active RhoA and cdc42 levels, modulated cytoskeletal rearrangement and increased invasion. We further determined that MDA-9 interacts with TGFβ1 via its PDZ1 domain. Finally, in vivo studies demonstrated that silencing the expression of MDA-9 resulted in decreased lung metastasis and TGFβ1 re-expression partially restored lung metastases. Our findings provide evidence for the relevance of MDA-9 in mediating EMT in breast cancer and support the potential of MDA-9 as a therapeutic target against metastatic disease.
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.