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Query: UMLS:C0025202 (melanoma)
 69,561 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

E-cadherin is a cell to cell adhesion molecule which acts as a suppressor of metastasis. This study examined the effect of gamma-linolenic acid (GLA), a n-6 polyunsaturated fatty acid, on the expression of E-cadherin in human cancer cells. Western blotting studies demonstrated that treatment of cells with GLA for 24 h increased the expression of E-cadherin in lung, colon, breast, melanoma, and liver cancer cells, but not in endothelial cells and fibroblasts. The results were confirmed by immunocytochemistry. In contrast, two other n-6 fatty acids, linoleic acid and arachidonic acid, failed to induce these changes. The increased expression of E-cadherin was correlated with reduced in vitro invasion and increased aggregation, indicating that the increased E-cadherin expression induced by GLA was biologically active. These data add GLA to the short list of E-cadherin up-regulatory factors. The up-regulation of E-cadherin expression in human cancer cells may contribute to the anticancer properties of GLA.
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PMID:Regulation of the expression of E-cadherin on human cancer cells by gamma-linolenic acid (GLA). 758 49

Melanoma often develops from clinically and histologically well-defined precursor lesions. During progression of normal melanocytes to benign nevi, dramatic changes in the expression of adhesion receptors are observed, most notably loss of E-cadherin which mediates adhesion of melanocytes to keratinocytes, and gain of Mel-CAM which predominantly mediates heterotypic adhesion between cells. Major changes in adhesion receptors also occur when cells progress from dysplastic nevi or biologically early radial-growth-phase primary melanomas to biologically late (tumorigenic) vertical-growth-phase primary melanomas. The integrin subunit beta 3 is up-regulated, whereas other integrins such as alpha 6 beta 1 and alpha V beta 1 are down-regulated. This review highlights the major changes in adhesion receptor expression on melanocytes at various stages of tumor progression.
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PMID:Adhesion receptors in human melanoma progression. 765 8

A human oral squamous-cell-carcinoma cell line, HOC313, was found to produce a factor which stimulates cell motility in an autocrine manner. The motility factor of HOC313 cells also promoted the locomotory activity of B16 murine melanoma cells reported to be sensitive to autocrine motility factor (AMF). HOC313 cells were found to express a large amount of AMF-receptor mRNA. In addition, the cell motility activity of HOC313 cells was completely blocked by pertussis toxin, a known inhibitor of AMF activity, suggesting that the motility factor of HOC313 cells may be AMF or a closely related factor. Immunocytochemical analysis has revealed that the AMF-like factor of HOC313 cells diminishes the cell-surface expression of adhesive molecule E-cadherin. These results suggest that down-regulation of E-cadherin may be involved in the cell-motility activity induced by the AMF-like factor of HOC313 cells.
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PMID:Identification and characterization of autocrine-motility-factor-like activity in oral squamous-cell-carcinoma cells. 798 19

E- and P-cadherin are calcium (Ca2+)-dependent cell adhesion molecules important in the morphogenesis and maintenance of skin structure. By use of flow cytometry and specific antibodies, we now show that cultured human melanocytes express E- and P-cadherin on their surfaces, and that these molecules have the same characteristics as reported for other cell types. Specifically, melanocyte cadherins are sensitive to trypsin digestion in the absence of Ca2+ and are protected from trypsin degradation by Ca2+, and are functional at 37 degrees C but not at 4 degrees C. We further show that melanocytes contain mRNA transcripts encoding both E- and P-cadherin. Adhesion of cultured melanocytes to keratinocyte monolayers is abolished by pre-treatment of the melanocytes with trypsin/EDTA, which degrades E- and P-cadherins, is greatly reduced by anti-E-cadherin antibodies and is slightly reduced by antibodies to P-cadherin, alpha 2, alpha 3 and beta 1 integrins. In contrast to normal melanocytes, eight of nine melanoma cell lines lacked E-cadherin (or expressed markedly reduced levels) and five were negative for P-cadherin. Melanoma cells also failed to adhere to keratinocyte monolayers. These results demonstrate that normal human melanocytes express functional E- and P-cadherin and that E-cadherin is primarily responsible for adhesion of human melanocytes to keratinocytes in vitro. In addition, transformed melanocytes express markedly reduced levels of E- and P-cadherin, and exhibit decreased affinity for normal keratinocytes in vitro, suggesting that loss of cadherins may play a role in melanoma metastasis.
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PMID:E-cadherin is the major mediator of human melanocyte adhesion to keratinocytes in vitro. 805 51

K-ras-NIH3T3 cells were more invasive than NIH3T3 cells in a chemotactic invasion assay. Conophylline, a new vinca alkaloid isolated as a ras function inhibitor, inhibited the invasion of K-ras-NIH3T3 cells, while it showed no effect on NIH3T3 cells. Conophylline did not increase expression of fibronectin but induced E-cadherin expression in K-ras-NIH3T3 cells. Mouse melanoma B16/F10 is a highly metastatic cell line. Conophylline was found to induce flat morphology in B16/F10 cells and it again inhibited the invasion of the cells to the matrigel membrane. It induced fibronectin expression but not E-cadherin expression in B 16/F10 cells. Thus, conophylline lowered invasiveness of K-ras-NIH3T3 and B 16/F10 cells by reversing neoplastic phenotypes.
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PMID:Inhibition of cellular chemotactic invasion by a vinca alkaloid, conophylline. 861 70

Introduction of the beta1-4 N-acetylglucosaminyltransferase (GnT-III) gene was reported to suppress metastasis in highly metastatic B16-hm murine melanoma cells (Yoshimura, M., Nishikawa, A. , Ihara, Y., Taniguchi, S., and Taniguchi, N.(1995) Proc. Natl. Acad. Sci. U. S. A. 92, 8754-8758). In this study, the effect of GnT-III gene transfer on E-cadherin was studied, since E-cadherin acts as a suppressor of metastasis. E-cadherin expression at cell-cell contacts of B16-hm cells expressing high GnT-III activity was greater than controls without affecting transcription. Lectin blotting showed that E-cadherin from GnT-III transfectants was glycosylated by ectopically expressed GnT-III. The glycosylated E-cadherin exhibited the delayed turnover and the decreased release from cell surface, as compared with the native E-cadherin, resulting in the elevated expression at the cell-cell border of GnT-III transfectants. Furthermore, cell-cell aggregation was enhanced in GnT-III transfectants, indicating that the glycosylated E-cadherin is biologically functional. These results suggest that the glycosylated E-cadherin contributes to the suppression of metastasis by the introduction of GnT-III gene into melanoma cells.
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PMID:Aberrant glycosylation of E-cadherin enhances cell-cell binding to suppress metastasis. 866 32

E-cadherin is a calcium-sensitive, cell-to-cell, adhesion molecule that is expressed widely in normal human epithelial tissue. Abnormal expression has been described in colorectal, breast and nasopharyngeal squamous cell carcinomas, where loss of E-cadherin is associated with an increased metastatic potential. We have examined, by standard immunohistochemical techniques using the monoclonal antibody HECD-1 (E-cadherin monoclonal antibody), the distribution of E-cadherin in normal human skin and in non-melanoma neoplastic lesions. In the normal epidermis, E-cadherin was strongly expressed on the surface of keratinocytes and specialized epithelial structures. Staining was absent from the lower pole of basal keratinocytes in contact with the basement membrane. Weak cytoplasmic staining was also noted in basal keratinocytes. No reactivity was demonstrated in dermal structures. The assessment of cutaneous tumours demonstrated an altered pattern of staining in most cases. Cell surface expression was reduced in 28 of 30 cases of basal cell carcinomas (BCC). Twenty showed an additional feature of positive staining on the dermal aspect of peripheral cells of tumour lobules. In squamous cell carcinomas (SCC) (n = 16), surface expression was attenuated in eight and absent in a further four. Strong surface expression, similar to normal skin was seen in all examples of Bowen's disease (n = 6), viral wart (n = 3), seborrhoeic keratosis (n = 3) and actinic keratosis (n = 4). This study demonstrates that, in BCC and SCC, but not in premalignant lesions, cell-surface expression of E-cadherin is reduced, consistent with the observation that the loss of E-cadherin is associated with tumour invasion.
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PMID:Expression of E-cadherin in human epidermal non-melanoma cutaneous tumours. 874 82

The purpose of our study was to determine whether the degree of E- and P-cadherin expression in melanomas correlates with the invasive behavior of the clinical lesions from which the cell lines were derived. Cadherins comprise a family of calcium-dependent cellular adhesion molecules expressed on most cell types that form solid tissues. In the human epidermis, melanocyte cadherin expression may function to maintain the integrity of the epidermal-melanin unit. Employing both immunofluorescence microscopy and fluorescence-activated cell sorter analysis, we localized and quantitated E- and P-cadherin expression on melanoma cell lines derived from primary or metastatic lesions using the monoclonal antibodies HECD-1 and NNC-CAD-299, respectively. Human epidermal melanocytes isolated from neonatal foreskin were evaluated by similar techniques and served as a biologic control. Melanoma cell lines were isolated from primary or metastatic lesions of patients described as having "early," "intermediate," or "advanced disease." Melanoma E- and P-cadherin immunofluorescence, as quantified by fluorescence-activated cell sorter, varied inversely with disease progression. Selected log mean ratios of E-cadherin fluorescence, as compared to human epidermal melanocytes (arbitrarily = 1), ranged from 1.04 in the WM 35 melanoma cell line (low invasive potential) to 0.1 and 0.02 in the WM 983A and 1361A melanoma cell lines (derived from primary lesions with metastases), respectively. Although values for P-cadherin fluorescence were less, the trend of decreasing cadherin amounts with more advanced disease was observed. Melanoma cells appear to express E- and P-cadherin levels inversely related to disease progression. Ultraviolet radiation significantly decreased E- and P-cadherin expression in the human epidermal melanocytes and P-cadherin expression in the WM 35 melanoma cell line (p < 0.05). Although not statistically significant, E-cadherin expression in the WM 35 melanoma cell line decreased substantially. Thus, ultraviolet radiation may have a direct effect on human epidermal melanocytes and melanoma cell attachment through cadherins within the epidermis or tumor nodules.
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PMID:Expression of E and P-cadherin by melanoma cells decreases in progressive melanomas and following ultraviolet radiation. 875 77

Loss of expression of E-cadherin, the major cell-cell adhesion receptor on keratinocytes, has been linked to tumour progression in various carcinomas. As E-cadherin has been reported to be expressed in cultured human melanocytes, we questioned whether loss of E-cadherin expression may also be related to melanocytic tumour progression. Flowcytometrical analysis demonstrated that E-cadherin was expressed on cultured normal melanocytes and naevus cells. Two non-invasive, non-metastatic melanoma cell lines showed low expression, and four invasive, metastatic melanoma cell lines did not express E-cadherin. Immunohistochemistry on frozen sections of human melanocytic lesions resulted in diffuse staining of 1/23 common naevocellular naevi and 1/13 dysplastic naevi, with no staining in any of seven early primary melanomas (< or = 1.5 mm). Staining was observed in 4/20 advanced primary melanomas (> 1.5 mm) and 5/35 melanoma metastases. Thus, even though E-cadherin is expressed in cultured melanocytes and naevus cells and lost in invasive, metastatic melanoma cells in vitro, it is rarely found in early stages of melanocytic tumour progression in situ and, surprisingly, some expression can be observed in 10-20% of lesions of advanced stages.
Melanoma Res 1996 Apr
PMID:E-cadherin expression in human melanoma. 879 Dec 70

The expression pattern of epithelial (E)- and placental (P)-calcium-dependent cell-cell adhesion molecules was examined immunohistochemically in various skin tumors. E- and P-cadherin expression was preserved in nodular and superficial types of basal cell carcinoma (BCC). In well-differentiated squamous cell carcinoma (SCC), E-cadherin on the cell surface of the tumor was reduced but expression of P-cadherin was preserved more frequently at the peripheral sites of the tumor than in the central sites of the tumor. Paget's cells and melanoma cells did not express E- or P-cadherins in the nest of the epidermis. Immunoreactive E-cadherin levels in sera were significantly elevated in patients with invasive Paget's disease, metastatic malignant melanoma and severe types of psoriasis and atopic dermatitis when compared with those of normal controls. Reduced or loss of cadherin in localized tumor cells may be correlated with the proliferation, and the level of soluble E-cadherin in circulation may be a marker in the extent of damaged skin by tumor and/or inflammation.
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PMID:E- and P-cadherin expression in tumor tissues and soluble E-cadherin levels in sera of patients with skin cancer. 890 51


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