ArticleMolecular biology of the cell2025
Deletion of the plexin-D1 ectodomain leads to anoikis by suppressing integrin inside-out signaling.
Article in Molecular biology of the cell, 2025. 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
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Plexin-D1, mainly expressed in endothelial and cancer cells, regulates diverse effects, suppresses endothelial cell growth, and induces cancer cell migration and proliferation. Here, we demonstrated that plexin-D1 was cleaved by proteinase on cancer cells. To examine the role of cleaved plexin-D1 in cells, Madin-Darby canine kidney (MDCK) cells overexpressing truncated plexin-D1 were cultured in Matrigel. MDCK cells expressing plexin-D1 lacking the ectodomain (plexin-D1 ΔEC) underwent apoptosis. An adhesion assay for extracellular matrix (ECM) molecules showed that plexin-D1 ΔEC-expressing MDCK cells lost their affinity for the ECM. These results suggest that plexin-D1 ΔEC blocks integrin inside-out signaling, leading to detachment from the ECM and apoptosis, so-called anoikis. By contrast, MDCK cells expressing full-length plexin-D1 or plexin-D1 lacking the cytoplasmic domain (plexin-D1 ΔIC) developed multicellular branching tubular structures in Matrigel. This morphological change was blocked in plexin-D1-expressing MDCK cells by the hepatocyte growth factor receptor (Met) loss of function or by Met inhibitors. These results suggest that plexin-D1 associates with Met through the plexin-D1 extracellular domain, and this activates Met cytoplasmic kinase activity. We therefore conclude that plexin-D1 contains distinct domains that determine the fate of cancer cells.
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.