E-cadherin as a functional marker of the differentiation and invasiveness of squamous cell carcinoma of the head and neck

Schipper, Jörg; Unger, Andreas; Jahnke, K.

doi:10.1111/j.1365-2273.1994.tb01252.x

Cited by 45 publications

(29 citation statements)

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“…Generally, however, reduced expression of E-cadherin is seen in aggressive, poorly differentiated tumors, with an infiltrative histological growth pattern (Pignatelli et a!., 1994;Schipper et al, 1994;Tamura et al, 1996). These observations are supported by in vitro assays where transfection of E-cadherin cDNA into deficient cells reduces invasiveness and tumorigenicity and increases cell adhesiveness and also down-regulates epidermal growth factor receptor (Vleminckx et al, 1991;Miyaki, 1995;Wilding et a!., 1996).…”

Section: Cadherins In Tumorssupporting

confidence: 52%

“…Positive correlations between reduced E-cadherin expression and increased incidence of lymph node metastases have been reported in various carcinomas, including pancreas, gastric, esophageal, breast, prostate, and head and neck (Matsuura Umbas et al, 1992;Miyata et al, 1994;Pignatelli et al, 1994;Schipper et al, 1994;Yamada et al, 1997). Murine ovarian carcinoma cells which strongly express E-cadherin show low metastatic potential (Hashimoto et al, 1989 (1994) carried out invasion assays using cell lines derived from tongue SCC.…”

Section: Cadherins In Tumorsmentioning

confidence: 99%

“…Occasionally, poorly differentiated tumors retain strong E-cadherin expression but lack E-cadherin function. This may be due to alterations in the catenin complex (Behrens et al, 1993), or mutation of the cadherin into a non-functioning form (Muta et al, 1996).Generally, however, reduced expression of E-cadherin is seen in aggressive, poorly differentiated tumors, with an infiltrative histological growth pattern (Pignatelli et a!., 1994;Schipper et al, 1994;Tamura et al, 1996). These observations are supported by in vitro assays where transfection of E-cadherin cDNA into deficient cells reduces invasiveness and tumorigenicity and increases cell adhesiveness and also down-regulates epidermal growth factor receptor (Vleminckx et al, 1991;Miyaki, 1995;Wilding et a!., 1996).…”

mentioning

confidence: 99%

“…These observations are supported by in vitro assays where transfection of E-cadherin cDNA into deficient cells reduces invasiveness and tumorigenicity and increases cell adhesiveness and also down-regulates epidermal growth factor receptor (Vleminckx et al, 1991;Miyaki, 1995;Wilding et a!., 1996). Conversely, blocking E-cadherin function in epithelial cells induces an invasive phenotype (Behrens et al, 1989).Positive correlations between reduced E-cadherin expression and increased incidence of lymph node metastases have been reported in various carcinomas, including pancreas, gastric, esophageal, breast, prostate, and head and neck (Matsuura Umbas et al, 1992;Miyata et al, 1994;Pignatelli et al, 1994;Schipper et al, 1994;Yamada et al, 1997). Murine ovarian carcinoma cells which strongly express E-cadherin show low metastatic potential (Hashimoto et al, 1989 (1994) carried out invasion assays using cell lines derived from tongue SCC.…”

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confidence: 99%

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Cell Adhesion Molecules and Oral Cancer

Thomas

Speight

2001

Critical Reviews in Oral Biology & Medicine

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Cell adhesion molecules (CAMs) are found on the surfaces of all cells, where they bind to extracellular matrix molecules or to receptors on other cells. As well as having a structural role, CAMs function as signaling receptors, transducing signals initiated by cellular interactions which regulate many diverse processes, including cell division, migration, and differentiation. Cell adhesion molecules are essential for maintaining stable tissue structure. However, cell adhesion must be dynamic to facilitate the mobility and turnover of cells. In dynamic situations, cells alter their cell-cell and cell-matrix interactions by virtue of altered expression and function of CAMs. The expression of CAMs is normally tightly regulated, thereby controlling cell proliferation, mobility, differentiation, and survival. Many of these processes are misregulated in malignant tumors, and it has been shown that many of the characteristics of tumor cells are attributable to the aberrant expression or function of CAMs.Integrins and E-cadherin are the most important CAMs expressed by stratified squamous epithelium. Altered expression of these molecules has been found in oral carcinoma, where loss of CAM expression is often seen in poorly differentiated lesions.However, up-regulation of certain integrins, such as av16, has consistently been found in oral cancer, suggesting that it may play an active role in disease progression.Key words. Oral cancer, cell adhesion molecules, integrins, cadherins, selectins, immunoglobulin superfamily, CD44. (I) IntroductionCell adhesion molecules (CAMs) are found on the surfaces of all cells, where they bind to extracellular matrix molecules or to receptors on other cells. Cell adhesion is critical in the dynamic processes necessary for tissue morphogenesis in development and the maintenance of complex differentiated tissues in adult organisms. CAMs serve in these roles by virtue of their capacity to connect the exterior of the cell with the interior. They form structural linkages between the cell cytoskeleton and the extracellular matrix or between cells, and also function as signaling receptors, transducing signals initiated by cellular interactions which regulate many diverse processes, including cell division, migration, and differentiation ( Fig. 1).Cell adhesion molecules are essential for maintaining the stable structure of stratified squamous epithelium. In normal epithelium, keratinocytes are attached to each other and to the underlying basement membrane. Cell adhesion, however, must be dynamic to facilitate the mobility and turnover of cells. In dynamic situations, keratinocytes alter their cell-cell and cell-ECM interactions by virtue of altered expression and function of CAMs.The expression of cell adhesion molecules is normally tightly regulated-forming, persisting, or declining in an ordered fashion. This allows for controlled cell proliferation, mobility, differentiation, and survival. Many of these processes are misregulated in malignant tumors, and it has been shown that man...

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Section: Cadherins In Tumorssupporting

confidence: 52%

Section: Cadherins In Tumorsmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Cell Adhesion Molecules and Oral Cancer

Thomas

Speight

2001

Critical Reviews in Oral Biology & Medicine

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“…17 Decreased levels of E-cadherin have also been associated with a metastatic phenotype in SCCHN cell lines. 18 This relationship has also been shown in tumor specimens, 19 indicating that loss of E-cadherin may be an important step in the development of metastasis in SCCHN.…”

Section: Fig 3 (A)mentioning

confidence: 81%

Change of E-Cadherin by Hepatocyte Growth Factor and Effects on the Prognosis of Hypopharyngeal Carcinoma

Kim

Kahng

et al. 2007

Ann Surg Oncol

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Background: Hepatocyte growth factor (HGF) is known to induce scattering in various epithelial cells, and E-cadherin plays important roles in the maintenance of cell-cell adhesion. However, the mechanisms surrounding these actions are not fully understood. Therefore, we examined how HGF affects the expression and distribution of E-cadherin. In addition, we observed the relationship between prognosis and modulation of E-cadherin by HGF in hypopharyngeal carcinoma.Methods: Tumor tissues from 66 patients with hypopharyngeal squamous cell carcinoma were evaluated for the expression of HGF, its receptor (c-Met), and E-cadherin. Reverse transcriptase-polymerase chain reaction (RT-PCR) and Western blot test were performed on hypopharyngeal cancer tissues. The association and changes of E-cadherin with HGF treatment in a hypopharyngeal cancer cell line were investigated by RT-PCR, Western blot analysis, inhibition assay, immunofluorescence staining, and invasion assay.Results: E-cadherin expression was found in 87.9% of squamous cell carcinomas; these could be further classified as membranous type (46.9%) or nonmembranous type (53.1%). The expression of HGF in tumors with nonmembranous type E-cadherin expression was far higher than in tumors with membranous expression. Nonmembranous type E-cadherin expression correlated significantly with lymph node metastasis, distant metastasis, and recurrence (P < .05). HGF decreased the expression of E-cadherin and induced the translocation of Ecadherin to the cytoplasm. HGF and E-cadherin neutralizing antibody stimulated dispersion, and HGF significantly enhanced the invasion of hypopharyngeal cancer cells in a dosedependent manner (P < .05).Conclusions: These results suggest that HGF can modulate the expression and intracellular localization of E-cadherin in hypopharyngeal cancer cells. In addition, these results indicate that changes in E-cadherin by HGF can affect the prognosis of hypopharyngeal carcinoma.

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Markers for Nodal Metastasis in Head and Neck Squamous Cell Cancer

Takes¹,

Jong²,

Alles³

et al. 2002

Arch Otolaryngol Head Neck Surg

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The expression of the investigated genetic markers and histopathological features of primary tumors can supply limited information on the metastatic behavior of tumors. Although the use of markers for regional metastasis would be a welcome additional tool, these results do not warrant the use of these parameters for clinical decision making concerning the treatment of the neck in patients with head and neck squamous cell cancer.

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E-cadherin as a functional marker of the differentiation and invasiveness of squamous cell carcinoma of the head and neck

Cited by 45 publications

References 12 publications

Cell Adhesion Molecules and Oral Cancer

Cell Adhesion Molecules and Oral Cancer

Change of E-Cadherin by Hepatocyte Growth Factor and Effects on the Prognosis of Hypopharyngeal Carcinoma

Markers for Nodal Metastasis in Head and Neck Squamous Cell Cancer

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