2012
DOI: 10.1074/jbc.m112.386235
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Epithelial Cell Adhesion Molecule Regulates Tumor Initiation and Tumorigenesis via Activating Reprogramming Factors and Epithelial-Mesenchymal Transition Gene Expression in Colon Cancer

Abstract: Background: EpCAM is highly expressed on tumor and tumor-initiating cells. Results: EpCAM induces reprogramming factor and EMT gene expression, which regulates tumor self-renewal and tumorigenesis. Conclusion: EpCAM-mediated self-renewal and initiation of tumor cells are regulated by inducing reprogramming factors expressions. Significance: Our data reveal the mechanism underlying EpCAM-mediated tumor initiation and tumorigenesis of tumorinitiating cells in colon cancer.

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Cited by 96 publications
(124 citation statements)
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“…It is thought to be involved in calcium-independent cell adhesion, signalling, migration, proliferation, and differentiation 1 extracellular domain (ex) with both epidermal growth factor and thyroglobulin repeat-like domains, a transmembrane domain, and a relatively short intracellular domain (icd) 2 . Proteolytic cleavage of epcam leads to the creation of an extracellular domain (epcam-ex) and an intracellular domain (epcam-icd) that consists of a short 26-amino-acid fragment that has been shown to trigger activation of the Wnt/beta-catenin pathway and aggressive tumour behavior 2,3 . In addition, formation of an epcam-icd-beta-catenin complex with other proteins has been shown to lead to transcription and upregulation of several genes, including c-Myc and CCND1, which might promote tumour growth 4 .…”
Section: Introductionmentioning
confidence: 99%
“…It is thought to be involved in calcium-independent cell adhesion, signalling, migration, proliferation, and differentiation 1 extracellular domain (ex) with both epidermal growth factor and thyroglobulin repeat-like domains, a transmembrane domain, and a relatively short intracellular domain (icd) 2 . Proteolytic cleavage of epcam leads to the creation of an extracellular domain (epcam-ex) and an intracellular domain (epcam-icd) that consists of a short 26-amino-acid fragment that has been shown to trigger activation of the Wnt/beta-catenin pathway and aggressive tumour behavior 2,3 . In addition, formation of an epcam-icd-beta-catenin complex with other proteins has been shown to lead to transcription and upregulation of several genes, including c-Myc and CCND1, which might promote tumour growth 4 .…”
Section: Introductionmentioning
confidence: 99%
“…Again, expression of EpCAM, just like CXCR4, is linked to the frequency of metastasis and tumor progression (40). Thus, the reduction of these characterized pathways clearly demonstrates the high activity of combinations of moguntinones with chemotherapeutic agents against tumor growth and progression, particularly in human colorectal cancer.…”
Section: Resultsmentioning
confidence: 97%
“…All affinitybased selections face the same inherent limitation of being (Cohen et al, 2008;Kumeria et al, 2012). This may be troubling considering that EpCAM is downregulated during the progression of epithelial-to-mesenchymal transition (EMT), in order to promote dissociation of potential future CTCs from tumor mass and invasion into the bloodstream (Gorges et al, 2012;Lin et al, 2012). Moreover, the type and expression levels of surface proteins may vary greatly in CTCs, depending on histological cancer subtype.…”
Section: Introductionmentioning
confidence: 98%