Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

The ECM and tissue architecture are major determinants of early invasion mediated by E-cadherin dysfunction

8 Nov 2023

Abstract excerpt

Germline mutations of E-cadherin cause Hereditary Diffuse Gastric Cancer (HDGC), a highly invasive cancer syndrome characterised by the occurrence of diffuse-type gastric carcinoma and lobular breast cancer. In this disease, E-cadherin-defective cells are detected invading the adjacent stroma since very early stages. Although E-cadherin loss is well established as a triggering event, other determinants of the...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Cancer Cells and Metastasis
Share to Cellular Mechanics and Interactions
Share to Polysaccharides and Plant Cell Walls

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 37938268
DOI: 10.1038/s42003-023-05482-x

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 8 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

The ECM and tissue architecture are major determinants of early invasion mediated by E-cadherin dysfunctionPMID 37938268Read ↗

Integrin β1 orchestrates the abnormal cell-matrix attachment and invasive behaviour of E-cadherin dysfunctional cellsSemantic proximity Read ↗

Cell division‐dependent dissemination following E‐cadherin loss underlies initiation of diffuse‐type gastric cancerSemantic proximity Read ↗

E-cadherin-defective gastric cancer cells depend on Laminin to survive and invadeSemantic proximity Read ↗

E-cadherin germline missense mutations and cell phenotype: evidence for the independence of cell invasion on the motile capabilities of the cells.Semantic proximity Read ↗

Basal extrusion drives cell invasion and mechanical stripping of E-cadherinSemantic proximity Read ↗

Escape from cell-cell and cell-matrix adhesion dependence underscores disease progression in gastric cancer organoid modelsSemantic proximity Read ↗

Dynamics of cell adhesion and motility in living cells is altered by a single amino acid change in E-cadherin fused to enhanced green fluorescent protein.Semantic proximity Read ↗

Extracellular domains of E-cadherin determine key mechanical phenotypes of an epithelium through cell- and non-cell-autonomous outside-in signaling.Semantic proximity Read ↗

Tumour-associated E-cadherin mutations alter cellular morphology, decrease cellular adhesion and increase cellular motility.Semantic proximity Read ↗

Loss of functional E-cadherin renders cells more resistant to the apoptotic agent taxol in vitro.Semantic proximity Read ↗

DNAJB4 molecular chaperone distinguishes WT from mutant E-cadherin, determining their fate in vitro and in vivo.Semantic proximity Read ↗

Anti-social cells: predicting the influence of E-cadherin loss on the growth of epithelial cell populations.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.