Normal epithelial cells express E-cadherin. However, tumor cells that have undergone an EMT begin to inappropriately express N-cadherin (neural cadherin). Expression of N-cadherin in mammary tumor cell lines leads to increased cell migration and invasion, regardless of E-cadherin expression (56, 57, 62). It has also been suggested that N-cadherin promotes breast cancer metastasis by reestablishing homophilic cell-cell adhesion in metastasis (57). In highly invasive breast tumors, N-cadherin was shown to replace E-cadherin at cell-cell contacts, and it has been proposed that N-cadherin mediates carcinoma cell interaction with mammary stromal and endothelial cells. Moreover, intravenous injection of MCF7 cells engineered to overexpress N-cadherin into nude mice results in increased metastasis, compared to parent MCF7 cells lacking N-cadherin. N-cadherin expression influences downstream signaling from the FGFR. Suyama et al., 2002, have implicated a direct interaction between N-cadherin and FGFR, resulting in receptor stabilization and prolonged signaling by FGF (59). N-cadherin-expressing breast carcinoma cells were specifically sensitized to FGF-2-induced invasion and upregulation of the proteolytic enzyme MMP-9. However, the findings are consistent with the observation that, although breast carcinoma cells expressing N-cadherin are more motile and invasive (57, 58) and many human breast cancers express N-cadherin, its presence does not correlate with poor survival (12, 63, 64). It is possible that additional events besides N-cadherin misexpression, such as overexpression of FGF or its receptor, decrease in E-cadherin expression, or increased levels of metal-loproteinases, are required to act in concert with N-cadherin to promote mammary tumor cell invasion and metastasis in vivo (11).

10 Ways To Fight Off Cancer

10 Ways To Fight Off Cancer

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