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Redistribution of β-catenin in response to EGF and lithium signalling in human oesophageal squamous carcinoma cell lines
BACKGROUND: The 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 met...
Autores principales: | , |
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Formato: | Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2003
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC194614/ https://www.ncbi.nlm.nih.gov/pubmed/12956888 http://dx.doi.org/10.1186/1475-2867-3-13 |
Sumario: | BACKGROUND: The 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). RESULTS: In 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. CONCLUSION: Therefore, 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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