ArticleFEBS open bio2026
Matrix metalloproteinase-9 regulates cell adhesion and membrane protrusive activity of ovarian cancer cells.
Article in FEBS open bio, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Matrix metalloproteinase-9 (MMP9), an extracellular endopeptidase, is upregulated by Epidermal Growth Factor (EGF) signaling and associated with ovarian epithelial cancer progression. To further understand the contribution of MMP9 to EGF-stimulated metastatic behavior, we created MMP9-null cells (M9-KO) from an ovarian cancer cell line. This model showed MMP9 loss did not block EGF-driven E-cadherin dissolution and associated epithelial-to-mesenchymal transition. However, MMP9-null cells exhibited delayed and reduced EGF-driven actin-based membrane protrusions, with transient re-expression of MMP9 sufficient to drive both lamellipodial and filopodial membrane protrusions. Finally, M9-KO cells exhibited a reduction of adhesion to extracellular matrices, which was significantly recovered by stable re-expression of MMP9. Together, these results provide direct evidence that MMP9 mediates EGF-driven membrane protrusions and promotes ovarian cancer cell adhesion to mesothelial extracellular matrices. Impact statement This work provides direct evidence that MMP9 mediates EGF-driven membrane protrusions and promotes ovarian cancer cell adhesion to mesothelial extracellular matrices.
Indexed as
Identifiers
What Socratic 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 Socratic graph.