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Posttranslational Truncation and Inactivation of Human E-Cadherin Distinguishes Prostate Cancer from Matched Normal Prostate¹

Department of Surgery, Section of Urology [M. G. R., M. G. S., C. J. V., J. R-D., M. A. R., M. L. D.], Cellular and Molecular Biology Graduate Program [J. R-D.], Department of Pathology [M. A. R.], and the University of Michigan Comprehensive Cancer Center [M. G. R., M. G. S., C. J. V., J. R-D., M. A. R., M. L. D.], University of Michigan, Ann Arbor, Michigan 48109-0944

An essential event in the progression of adenocarcinoma is the loss of organized epithelial attachment (both to the basement membrane and to adjoining epithelial cells). The E-cadherin cell adhesion molecule has an established function in maintaining normal phenotype and tissue homeostasis, and loss of E-cadherin function has been implicated in tumorigenesis. Aberrations in E-cadherin are associated with prostate cancer progression; however, these aberrations are not simply a result of prodigious allelic loss. We have previously demonstrated a novel posttranslational truncation within the cytosolic domain of native M_r 120,000 E-cadherin to a membrane-bound M_r 97,000 species. We hypothesize that truncation of E-cadherin is an inactivating event that is significantly increased in localized prostate tumors and that it represents a novel molecular event that may distinguish prostate cancer from adjacent normal tissue. E-cadherin was characterized by Western blot analysis in matched normal and cancer tissue from 18 prostate cancer patients. Imaging and densitometry software were used to quantify the truncation of E-cadherin by measuring the ratio of M_r 97,000 E-cadherin to M_r 120,000 E-cadherin, which was significantly increased in the tumor aspect of the prostate gland. Herein, we report the first experiment comparing case-matched human normal and cancerous prostate tissue in the context of E-cadherin truncation.

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