ArticleCancer cell international2003
Redistribution of β-catenin in response to EGF and lithium signalling in human oesophageal squamous carcinoma cell lines.
Article in Cancer cell international, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
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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.
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Who cites it
1 citing paper in PubMed, 5 citations in OpenAlex.
- Role of Cell-Cell Junctions in Oesophageal Squamous Cell Carcinoma.Biomolecules · 2022Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe β-catenin link between membrane-bound cadherins and the actin cytoskeleton regulates cell adhesion and consequently metastasis. Abnormal stabilisation of β-catenin enhances its transcriptional activities. Factors affecting β-catenin's functions are important in understanding metastatic diseases such as oesophageal squamous cell carcinoma (SCC).
resultsIn human oesophageal SCCs β-catenin localises predominantly to the plasma membrane. The presence of free β-catenin in the cytoplasm/nucleus was low. This indicates that β-catenin's activities are skewed towards cell-cell adhesion in these oesophageal SCCs. Exposure to EGF or Li alone, produced a slight increase in membrane concentrations but only Li induced β-catenin stabilisation in the cytoplasm. In combination, EGF and Li decreased membrane-associated β-catenin, concomitantly increasing cytoplasmic concentrations. Convergence of these signalling pathways appears to induce a β-catenin shift from the membrane into the cytoplasm.
conclusionTherefore, although the adhesive role of β-catenin appears to be intact, exogenous signals increase the stability of free β-catenin thereby reducing cell-cell adhesion in these tumours.
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Registered trials
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