Truncated E-cadherin potentiates cell death in prostate epithelial cells

BACKGROUND. E-cadherin, a fundamental component of the adherens junction, is known to mediate aggregation-dependent cell survival. We have previously identified a novel, calpain-dependent proteolytic cleavage of E-cadherin that resulted in the generation of a stable 100-kDa E-cadherin fragment (E-cad(100)) in prostate epithelial cells in response to cell death stimuli. We postulated that the E-cad(100) fragment may play a role in abrogating survival of LNCaP cells following induction of apoptosis. METHODS. Wild-type E-cadherin and E-cad(100) were engineered, tagged with GFP, and stably expressed in LNCaP cells. These cell lines were characterized for E-cadherin-GFP/beta-catenin interactions, endogenous E-cadherin and (beta-catenin expression, and sensitivity to apoptosis induced by PKC activation.