A Defect in Cell-to-cell Adhesion via Integrin-Fibronectin Interactions in a Highly Metastatic Tumor Cell Line

We examined the expression of the neural cell adhesion molecule NCAM in a number of endocrine tissues of adult rat and in an endocrine tumor cell line. NCAM was found by immunoelectron microscopy to be present on the surface of all endocrine cells in the three lobes of the hypophysis, although staining was relatively less intense in the intermediate lobe, and in pancreatic islets. Pituicytes, hypophyseal glial cells, were also labeled for NCAM. A rat insulinoma cell line (RIN A2) also expressed NCAM as judged by immunocytochemistry. Analysis of NCAM antigenic determinants (Mr 180, 140, and 120 KD) revealed large variations in the relative proportions of NCAM polypeptides present in the different tissues. Although all tissues and cell lines expressed NCAM-140, NCAM-180 was not detected in the adenohypophysis, pancreas, or adrenal medulla, and NCAM-120 was found in none of the endocrine tissues or cell lines except at low levels in the neurohypophysis. The tumor cell line expressed significant levels of NCAM-180, which was most abundant in the neurohypophysis. These results show that NCAM expression appears to be a general property of endocrine cells, although the antigenic composition differs markedly from that in brain tissue. These data are discussed with regard to the embryological origins of the different endocrine tissues, and possible functional implications are suggested.

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An Intravital Model to Monitor Steps of Metastatic Tumor Cell Adhesion Within the Hepatic Microcirculation

Journal of Gastrointestinal Surgery ◽

10.1016/s1091-255x(03)00023-4 ◽

2003 ◽

Vol 7 (4) ◽

pp. 507-515 ◽

Cited By ~ 57

Author(s):

J Haier

Keyword(s):

Cell Adhesion ◽

Tumor Cell ◽

Metastatic Tumor ◽

Tumor Cell Adhesion ◽

Hepatic Microcirculation ◽

Metastatic Tumor Cell

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Stromal fibroblasts induce metastatic tumor cell clusters via epithelial–mesenchymal plasticity

Life Science Alliance ◽

10.26508/lsa.201900425 ◽

2019 ◽

Vol 2 (4) ◽

pp. e201900425 ◽

Cited By ~ 11

Author(s):

Yuko Matsumura ◽

Yasuhiko Ito ◽

Yoshihiro Mezawa ◽

Kaidiliayi Sulidan ◽

Yataro Daigo ◽

...

Keyword(s):

Cell Adhesion ◽

Tumor Cell ◽

Transforming Growth Factor ◽

Cluster Formation ◽

Metastatic Tumor ◽

M Cells ◽

Stromal Fibroblasts ◽

Cell Clusters ◽

Metastatic Tumor Cell ◽

E Cadherin

Emerging evidence supports the hypothesis that multicellular tumor clusters invade and seed metastasis. However, whether tumor-associated stroma induces epithelial–mesenchymal plasticity in tumor cell clusters, to promote invasion and metastasis, remains unknown. We demonstrate herein that carcinoma-associated fibroblasts (CAFs) frequently present in tumor stroma drive the formation of tumor cell clusters composed of two distinct cancer cell populations, one in a highly epithelial (E-cadherinhiZEB1lo/neg: Ehi) state and another in a hybrid epithelial/mesenchymal (E-cadherinloZEB1hi: E/M) state. The Ehi cells highly express oncogenic cell–cell adhesion molecules, such as carcinoembryonic antigen-related cell adhesion molecule 5 (CEACAM5) and CEACAM6 that associate with E-cadherin, resulting in increased tumor cell cluster formation and metastatic seeding. The E/M cells also retain associations with Ehi cells, which follow the E/M cells leading to collective invasion. CAF-produced stromal cell-derived factor 1 and transforming growth factor-β confer the Ehi and E/M states as well as invasive and metastatic traits via Src activation in apposed human breast tumor cells. Taken together, these findings indicate that invasive and metastatic tumor cell clusters are induced by CAFs via epithelial–mesenchymal plasticity.

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