E-cadherin is a cell adhesion molecule expressed in epithelial cells. The cell-cell adhesion function of E-cadherin has been implicated in regulating cell polarity and junctional complexes in epithelial cells. In variety of cancers derived from epithelial cells E-cadherin expression/function is lost. Re-expression of E-cadherin in cancer cells to a large extent suppresses invasive tumor growth and hence E-cadherin has been termed as an invasion suppressor. A soluble form of E-cadherin (SECAD) has recently been identified in the serum of cancer patients and is associated with poor prognosis. The physiological significance of SECAD has not been investigated. In this proposal using various cell and molecular biological approaches I aim to study physiological role of SECAD in epithelial cell signaling. These studies should provide novel insights into mechanisms of SECAD function in normal and transformed epithelial cells.
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