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.

Agency
National Institute of Health (NIH)
Institute
National Institute of General Medical Sciences (NIGMS)
Type
Predoctoral Individual National Research Service Award (F31)
Project #
5F31GM068985-04
Application #
7117246
Study Section
Special Emphasis Panel (ZRG1-F05 (29))
Program Officer
Gaillard, Shawn R
Project Start
2003-09-01
Project End
2007-05-31
Budget Start
2006-09-01
Budget End
2007-05-31
Support Year
4
Fiscal Year
2006
Total Cost
$23,077
Indirect Cost
Name
University of California Los Angeles
Department
Pathology
Type
Schools of Medicine
DUNS #
092530369
City
Los Angeles
State
CA
Country
United States
Zip Code
90095
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Inge, Landon J; Rajasekaran, Sigrid A; Wolle, Daniel et al. (2008) alpha-Catenin overrides Src-dependent activation of beta-catenin oncogenic signaling. Mol Cancer Ther 7:1386-97
Inge, L J; Rajasekaran, S A; Yoshimoto, K et al. (2008) Evidence for a potential tumor suppressor role for the Na,K-ATPase beta1-subunit. Histol Histopathol 23:459-67