Poorly Differentiated Colon Carcinoma Cell Lines Deficient in α-Catenin Expression Express High Levels of Surface E-cadherin but Lack Ca2+-Dependent Cell-Cell Adhesion

The ability of carcinomas to invade and to metastasize largely depends on the degree of epithelial differentiation within the tumors, i.e., poorly differentiated being more invasive than well-differentiated carcinomas. Here we confirmed this correlation by examining various human cell lines derived from bladder, breast, lung, and pancreas carcinomas. We found that carcinoma cell lines with an epithelioid phenotype were noninvasive and expressed the epithelium-specific cell-cell adhesion molecule E-cadherin (also known as Arc-1, uvomorulin, and cell-CAM 120/80), as visualized by immunofluorescence microscopy and by Western and Northern blotting, whereas carcinoma cell lines with a fibroblastoid phenotype were invasive and had lost E-cadherin expression. Invasiveness of these latter cells could be prevented by transfection with E-cadherin cDNA and was again induced by treatment of the transfected cells with anti-E-cadherin mAbs. These findings indicate that the selective loss of E-cadherin expression can generate dedifferentiation and invasiveness of human carcinoma cells, and they suggest further that E-cadherin acts as an invasion suppressor.

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Repression of Na,K-ATPase β1-Subunit by the Transcription Factor Snail in Carcinoma

Molecular Biology of the Cell ◽

10.1091/mbc.e03-09-0646 ◽

2004 ◽

Vol 15 (3) ◽

pp. 1364-1373 ◽

Cited By ~ 73

Author(s):

Cromwell E. Espineda ◽

Jay H. Chang ◽

Jeffery Twiss ◽

Sigrid A. Rajasekaran ◽

Ayyappan K. Rajasekaran

Keyword(s):

Transcription Factor ◽

Cell Lines ◽

Carcinoma Cell ◽

Ectopic Expression ◽

Α Subunit ◽

Mesenchymal Transition ◽

Carcinoma Cell Lines ◽

Poorly Differentiated Carcinoma ◽

Poorly Differentiated ◽

E Cadherin

The Na,K-ATPase consists of two essential α- and β-subunits and regulates the intracellular Na+ and K+ homeostasis. Although the α-subunit contains the catalytic activity, it is not active without functional β-subunit. Here, we report that poorly differentiated carcinoma cell lines derived from colon, breast, kidney, and pancreas show reduced expression of the Na,K-ATPase β1-subunit. Decreased expression of β1-subunit in poorly differentiated carcinoma cell lines correlated with increased expression of the transcription factor Snail known to down-regulate E-cadherin. Ectopic expression of Snail in well-differentiated epithelial cell lines reduced the protein levels of E-cadherin and β1-subunit and induced a mesenchymal phenotype. Reduction of Snail expression in a poorly differentiated carcinoma cell line by RNA interference increased the levels of Na,K-ATPase β1-subunit. Furthermore, Snail binds to a noncanonical E-box in the Na,K-ATPase β1-subunit promoter and suppresses its promoter activity. These results suggest that down-regulation of Na,K-ATPase β1-subunit and E-cadherin by Snail are associated with events leading to epithelial to mesenchymal transition.

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Expression of the cell–cell adhesion molecule E-cadherin in tongue carcinoma cell lines

The Journal of Laryngology & Otology ◽

10.1017/s0022215100128622 ◽

1994 ◽

Vol 108 (11) ◽

pp. 957-961 ◽

Cited By ~ 7

Author(s):

A. R. Kinsella ◽

G. L. Bowie ◽

J. K. Fields ◽

A. S. Jones

Keyword(s):

Cell Adhesion ◽

Cell Line ◽

Cell Lines ◽

Adhesion Molecule ◽

Cell Adhesion Molecule ◽

Carcinoma Cell ◽

Tumour Progression ◽

Tongue Carcinoma ◽

Carcinoma Cell Lines ◽

E Cadherin

AbstractA reduction in cell adhesiveness and cell invasion are essential steps in tumour progression. In the present study six tongue carcinoma cell lines were compared with regard to their invasive potential in two in vitro invasion assay systems and for their patterns of expression of the cell–cell adhesion molecule E-cadherin. The three cell lines negative for E-cadherin expression were invasive in both assays. One cell line with strong E-cadherin expression was strongly invasive and one weakly invasive. One cell line with reduced E-cadherin expression was weakly invasive. There was no significant pattern to these findings (x2 = 0.375; p = 0.54). This supports previous studies from this group that suggest that E-cadherin is only one of the presumably many molecules involved in tumour progression in squamous cell carcinoma of the tongue.

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Modulation of EGF Receptor Expression by Differentiating Agents in Human Colon Carcinoma Cell Lines

Cancer Communications ◽

10.3727/095535490820874092 ◽

1990 ◽

Vol 2 (10) ◽

pp. 345-355 ◽

Cited By ~ 24

Author(s):

Lizabeth Deutsch Murphy ◽

Eva M. Valverius ◽

Maria Tsokos ◽

Lyn A. Mickley ◽

Neal Rosen ◽

...

Keyword(s):

Colon Carcinoma ◽

Cell Lines ◽

Egf Receptor ◽

Carcinoma Cell ◽

Human Colon ◽

Receptor Expression ◽

Human Colon Carcinoma Cell ◽

Carcinoma Cell Lines ◽

Human Colon Carcinoma ◽

Differentiating Agents

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Cytometric Profiling of CD133+ Cells in Human Colon Carcinoma Cell Lines Identifies a Common core Phenotype and Cell Type-specific Mosaics

The International Journal of Biological Markers ◽

10.5301/jbm.5000020 ◽

2013 ◽

Vol 28 (3) ◽

pp. 267-273 ◽

Cited By ~ 11

Author(s):

Marica Gemei ◽

Rosa Di Noto ◽

Peppino Mirabelli ◽

Luigi Del Vecchio

Keyword(s):

Colorectal Cancer ◽

Stem Cells ◽

Cancer Stem Cells ◽

Colon Carcinoma ◽

Cell Lines ◽

Carcinoma Cell ◽

Cell Type ◽

Carcinoma Cell Lines ◽

Cell Type Specific

In colorectal cancer, CD133+ cells from fresh biopsies proved to be more tumorigenic than their CD133– counterparts. Nevertheless, the function of CD133 protein in tumorigenic cells seems only marginal. Moreover, CD133 expression alone is insufficient to isolate true cancer stem cells, since only 1 out of 262 CD133+ cells actually displays stem-cell capacity. Thus, new markers for colorectal cancer stem cells are needed. Here, we show the extensive characterization of CD133+ cells in 5 different colon carcinoma continuous cell lines (HT29, HCT116, Caco2, GEO and LS174T), each representing a different maturation level of colorectal cancer cells. Markers associated with stemness, tumorigenesis and metastatic potential were selected. We identified 6 molecules consistently present on CD133+ cells: CD9, CD29, CD49b, CD59, CD151, and CD326. By contrast, CD24, CD26, CD54, CD66c, CD81, CD90, CD99, CD112, CD164, CD166, and CD200 showed a discontinuous behavior, which led us to identify cell type-specific surface antigen mosaics. Finally, some antigens, e.g. CD227, indicated the possibility of classifying the CD133+ cells into 2 subsets likely exhibiting specific features. This study reports, for the first time, an extended characterization of the CD133+ cells in colon carcinoma cell lines and provides a “dictionary” of antigens to be used in colorectal cancer research.

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Corrigendum to “Design and synthesis of functionalized glycomers as non-peptidic ligands for SH2 binding and as inhibitors of A-431 human epidermoid and HT-29 colon carcinoma cell lines” [Bioorg. Med. Chem. Lett. 10 (2000) 439]†

Bioorganic & Medicinal Chemistry Letters ◽

10.1016/s0960-894x(00)00554-0 ◽

2000 ◽

Vol 10 (23) ◽

pp. 2691

Author(s):

Stephen Hanessian ◽

Oscar M Saavedra ◽

Fang Xie ◽

Nadia Amboldi ◽

Carlo Battistini

Keyword(s):

Colon Carcinoma ◽

Cell Lines ◽

Carcinoma Cell ◽

Design And Synthesis ◽

Carcinoma Cell Lines ◽

Ht 29

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Reevaluating αE-catenin monomer and homodimer functions by characterizing E-cadherin/αE-catenin chimeras

The Journal of Cell Biology ◽

10.1083/jcb.201411080 ◽

2015 ◽

Vol 210 (7) ◽

pp. 1065-1074 ◽

Cited By ~ 18

Author(s):

Julie M. Bianchini ◽

Khameeka N. Kitt ◽

Martijn Gloerich ◽

Sabine Pokutta ◽

William I. Weis ◽

...

Keyword(s):

Cell Adhesion ◽

Intercellular Adhesion ◽

Dependent Cell ◽

In Cells ◽

E Cadherin ◽

Cell Cell

As part of the E-cadherin–β-catenin–αE-catenin complex (CCC), mammalian αE-catenin binds F-actin weakly in the absence of force, whereas cytosolic αE-catenin forms a homodimer that interacts more strongly with F-actin. It has been concluded that cytosolic αE-catenin homodimer is not important for intercellular adhesion because E-cadherin/αE-catenin chimeras thought to mimic the CCC are sufficient to induce cell–cell adhesion. We show that, unlike αE-catenin in the CCC, these chimeras homodimerize, bind F-actin strongly, and inhibit the Arp2/3 complex, all of which are properties of the αE-catenin homodimer. To more accurately mimic the junctional CCC, we designed a constitutively monomeric chimera, and show that E-cadherin–dependent cell adhesion is weaker in cells expressing this chimera compared with cells in which αE-catenin homodimers are present. Our results demonstrate that E-cadherin/αE-catenin chimeras used previously do not mimic αE-catenin in the native CCC, and imply that both CCC-bound monomer and cytosolic homodimer αE-catenin are required for strong cell–cell adhesion.

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