2007
DOI: 10.1158/0008-5472.can-06-3259
|View full text |Cite
|
Sign up to set email alerts
|

E-Cadherin Cell-Cell Adhesion in Ewing Tumor Cells Mediates Suppression of Anoikis through Activation of the ErbB4 Tyrosine Kinase

Abstract: Ability to grow under anchorage-independent conditions is one of the major hallmarks of transformed cells. Key to this is the capacity of cells to suppress anoikis, or programmed cell death induced by detachment from the extracellular matrix. To model this phenomenon in vitro, we plated Ewing tumor cells under anchorage-independent conditions by transferring them to dishes coated with agar to prevent attachment to underlying plastic. This resulted in marked up-regulation of E-cadherin and rapid formation of mu… Show more

Help me understand this report
View preprint versions

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
1
1

Citation Types

15
157
0

Year Published

2008
2008
2015
2015

Publication Types

Select...
8

Relationship

1
7

Authors

Journals

citations
Cited by 162 publications
(172 citation statements)
references
References 61 publications
15
157
0
Order By: Relevance
“…In contrast, downregulation of E-cadherin function causes reduced viability, suggesting that proliferation signals downstream of E-cadherin activation contribute to ovarian cancer cell survival. Similar results have been observed in squamous cell carcinoma [89], hepatoma [90] and Ewing tumor cells [91].…”
Section: Functional Impact Of Phenotypic Plasticity: Why Gain E-cadhesupporting
confidence: 87%
See 1 more Smart Citation
“…In contrast, downregulation of E-cadherin function causes reduced viability, suggesting that proliferation signals downstream of E-cadherin activation contribute to ovarian cancer cell survival. Similar results have been observed in squamous cell carcinoma [89], hepatoma [90] and Ewing tumor cells [91].…”
Section: Functional Impact Of Phenotypic Plasticity: Why Gain E-cadhesupporting
confidence: 87%
“…This phenomenon has been attributed to limited drug penetration, reduced fractions of proliferating cells, and enhanced resistance to detachment-induced apoptosis (anoikis) [98]. Disruption of E-cadherin-mediated cell adhesion in spheroids sensitizes tumor cells to chemotherapeutic agents [91,94]. This property of chemoresistance is also observed in ovarian tumor spheroids.…”
mentioning
confidence: 99%
“…Similarly in HT29 cells as reported, colony formation ability diminished remarkably after E-cadherin was blocked by SHE 78-7 [32] . Consistently, it is reported that Ewing tumor cells transfected by a dominant negative form of E-cadherin plasmid formed fewer and significantly smaller colonies compared with non-transduced cells [27] . Therefore, further research needs to be performed to try to elucidate the exact function of E-cadherin in ovarian cancer development and progression, especially the relationship between its contrary roles in regulating cell mobility and cell viability.…”
Section: Wwwchinapharcom Dong Ll Et Alsupporting
confidence: 68%
“…The E-cadherin expression is diminished at later stages of tumor progression as cells de-differentiate and acquire mesenchymal properties associated with a more aggressive phenotype [23][24][25] . Furthermore, a growing volume of data indicate that cell-cell adhesion mediated by E-cadherin is involved in the suppression of anoikis and maintenance of cellular survival in both epithelial cells, such as normal enterocytes [26] , oral squamous carcinoma cells [12] and nonepithelia such as Ewing tumor cells [27] . Instead of distant hematogenous metastasis like most other tumors, regional growth and superficial invasion restricted in the peritoneal cavity are the prominent characteristics of ovarian epithelial cancer.…”
Section: Wwwchinapharcom Dong Ll Et Almentioning
confidence: 99%
“…It was found that E-cadherin binding could activate intracellular proliferation and survival signals by activating the survival-associated mitogen activated protein kinase (MAPK) and Akt/PKB cascades via the classical Raf-MEK-MAPK pathway and PI3K, respectively (89). Moreover, it was found that E-cadherin cell-cell adhesion suppressed anoikis and increased the resistance of cells to cytotoxic agents by activating ErbB4, which also led to induction of the PI3K-Akt pathway (90). The exact mechanisms of this process and more related signals require further investigation.…”
Section: Survival Advantage Of Cancer Cells With Metmentioning
confidence: 99%