ArticleeLife2015
Defective apical extrusion signaling contributes to aggressive tumor hallmarks.
Article in eLife, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 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
46 citing papers in PubMed, 74 citations in OpenAlex.
- Starvation improves epithelial fitness by selectively extruding DNA damaged cells.bioRxiv : the preprint server for biology · 2026Article
- Anoikis resistance and cancer.BMC cancer · 2025Review
- Epithelial guardians against cancer: integrating cell competition and extrusion in early tumor control.Discover oncology · 2025Review
- Basal Invasion of Cancer Cells Driven by Cell-Cell Interactions: An Affirmative Role of Cell Competition in Cancer Progression.Cancer science · 2025Review
- Role of Sphingosine-1-Phosphate Signaling Pathway in Pancreatic Diseases.International journal of molecular sciences · 2024Review
- A sphingolipid rheostat controls apoptosis versus apical cell extrusion as alternative tumour-suppressive mechanisms.Cell death & disease · 2024Article
- Mechanism of efferocytosis in atherosclerosis.Journal of molecular medicine (Berlin, Germany) · 2024Review
- Loss of EGF receptor polarity enables homeostatic imbalance in epithelial-cell models.Molecular biology of the cell · 2023Article
- Bidirectional multiciliated cell extrusion is controlled by Notch-driven basal extrusion and Piezo1-driven apical extrusion.Development (Cambridge, England) · 2023Article
- Article
- Expanding roles of centrosome abnormalities in cancers.BMB reports · 2023Review
- Article
- Bidirectional multiciliated cell extrusion is controlled by Notch driven basal extrusion and Piezo 1 driven apical extrusion.bioRxiv : the preprint server for biology · 2023Article
- Ha-RasBiomedicines · 2022Article
- Impact of Epithelial Cell Shedding on Intestinal Homeostasis.International journal of molecular sciences · 2022Review
- Stromal architecture directs early dissemination in pancreatic ductal adenocarcinoma.JCI insight · 2022Article
- Uncovering the 'sphinx' of sphingosine 1-phosphate signalling: from cellular events to organ morphogenesis.Biological reviews of the Cambridge Philosophical Society · 2022Review
- ECM-transmitted shear stress induces apoptotic cell extrusion in early breast gland development.Frontiers in cell and developmental biology · 2022Article
- KRas-transformed epithelia cells invade and partially dedifferentiate by basal cell extrusion.Nature communications · 2021Article
- EPHA2-dependent outcompetition of KRASG12D mutant cells by wild-type neighbors in the adult pancreas.Current biology : CB · 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
8 authors at 3 institutions in 1 country.
Funding
Abstract
When epithelia become too crowded, some cells are extruded that later die. To extrude, a cell produces the lipid, Sphingosine 1-Phosphate (S1P), which activates S1P₂ receptors in neighboring cells that seamlessly squeeze the cell out of the epithelium. Here, we find that extrusion defects can contribute to carcinogenesis and tumor progression. Tumors or epithelia lacking S1P₂ cannot extrude cells apically and instead form apoptotic-resistant masses, possess poor barrier function, and shift extrusion basally beneath the epithelium, providing a potential mechanism for cell invasion. Exogenous S1P₂ expression is sufficient to rescue apical extrusion, cell death, and reduce orthotopic pancreatic tumors and their metastases. Focal Adhesion Kinase (FAK) inhibitor can bypass extrusion defects and could, therefore, target pancreatic, lung, and colon tumors that lack S1P₂ without affecting wild-type tissue.
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.