2008
DOI: 10.1016/j.canlet.2008.02.058
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A novel function of CD82/KAI-1 on E-cadherin-mediated homophilic cellular adhesion of cancer cells

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Cited by 62 publications
(73 citation statements)
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“…The results of the in vitro invasion assay showed a significant induction of cancer cell dissemination from the primary tumor nests in the ACCS-M GFP cell line. As this assay evaluates E-cadherin-mediated tumor cell dissemination (14), these data support the invasive and metastatic character of the primary implanted tumor of ACCS-M GFP in vivo and suggest that molecular alteration of cell adhesion molecules occurs on ACCS-M GFP cell surfaces. One explanation for the success of in vivo selection and changes in metastatic character is the inherent genetic heterogeneity of malignant cells.…”
Section: Discussionsupporting
confidence: 59%
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“…The results of the in vitro invasion assay showed a significant induction of cancer cell dissemination from the primary tumor nests in the ACCS-M GFP cell line. As this assay evaluates E-cadherin-mediated tumor cell dissemination (14), these data support the invasive and metastatic character of the primary implanted tumor of ACCS-M GFP in vivo and suggest that molecular alteration of cell adhesion molecules occurs on ACCS-M GFP cell surfaces. One explanation for the success of in vivo selection and changes in metastatic character is the inherent genetic heterogeneity of malignant cells.…”
Section: Discussionsupporting
confidence: 59%
“…Tumor dissemination potential from the primary cancer nest was evaluated by an in vitro invasion assay, as described previously (14). briefly, 1x10…”
Section: Accs Metastatic Orthotopic Implantation Mouse Model and In Vmentioning
confidence: 99%
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“…The question as to how CD82, a tumor suppressor protein, mediates xenorecognition is yet to be addressed. Tumor metastasis suppression by CD82 is thought to occur by stabilizing E-cadherin/b-catenin complex formation (66), upregulation of Sprouty2 (67), maturation of b 1 -integrin (68), and direct interactions with the Duffy Ag/receptor for chemokine-expressing endothelial cells (69). Whether such mechanisms could be exploited for increased survival of a xenograft remains to be addressed.…”
Section: Discussionmentioning
confidence: 99%
“…CD82 inhibits fibronectin adhesion-induced epithelial-to-mesenchymal transition in prostate cancer cells by repressing the associated integrin signaling [3], and CD44 alternative splicing-dependent melanoma metastasis by mediating U2AF2 ubiquitination and degradation [4]. Abe et al [5] found that CD82 strengthened E-cadherin-mediated intercellular adhesion, stabilized E-cadherin/ β-catenin complex formation, and reduced tyrosine phosphorylation of β-catenin on HGF stimulation. CD82 specifically suppressed ubiquitylation of EGFR after stimulation with heparin-binding EGF or amphiregulin [6], and attenuated compartmentalisation and ligand-induced dimerization of EGFR [7].…”
Section: Introductionmentioning
confidence: 99%