Abstract
Expression of δ-catenin reportedly increases during late stage prostate cancer. Furthermore, it has been demonstrated that expression of EGFR is enhanced in hormone refractory prostate cancer. In this study, we investigated the possible correlation between EGFR and δ-catenin in prostate cancer cells. We found that EGFR interacted with δ-catenin and the interaction decreased in the presence of EGF. We also demonstrated that, on one hand, EGFR phosphorylated δ-catenin in a Src independent manner in the presence of EGF and on the other hand, δ-catenin enhanced protein stability of EGFR and strengthened the EGFR/Erk1/2 signaling pathway. Our findings added a new perspective to the interaction of EGFR to the E-cadherin complex. They also provided novel insights to the roles of δ-catenin in prostate cancer cells.
Highlights
Expression of δ-catenin reportedly increases during late stage prostate cancer
While Epidermal growth factor receptor (EGFR) is up-regulated by Fbw-7 (F-box and WD repeat domain-containing 7), an ubiquitin ligase, and hypoxic condition[5,6], it is down-regulated through various mechanisms, among which clathrin-dependent endocytosis, presenilin-1 and caspase-3 regulation are well studied[7,8,9,10]
We found that EGFR was detected in the purified δ -catenin immune-complex and interestingly, the interaction was reduced in response to EGF treatment (Fig. 2A)
Summary
Expression of δ-catenin reportedly increases during late stage prostate cancer. it has been demonstrated that expression of EGFR is enhanced in hormone refractory prostate cancer. On one hand, EGFR phosphorylated δ-catenin in a Src independent manner in the presence of EGF and on the other hand, δ-catenin enhanced protein stability of EGFR and strengthened the EGFR/Erk1/2 signaling pathway. Our findings added a new perspective to the interaction of EGFR to the E-cadherin complex They provided novel insights to the roles of δ-catenin in prostate cancer cells. EGF-EGFR was reported to mainly phosphorylate p120ctn on its Y228 residue in a Src independent manner. We currently investigated the relationship between δ -catenin and EGFR in order to delineate the potential connection between the enhanced EGFR expression in hormone refractory prostate cancer and the reciprocity of increased δ -catenin and decreased p120ctn expression during late stage prostate cancer. Our data indicated that δ -catenin stabilized EGFR protein expression and enhanced the EGFR/Ek1/2 signaling pathway
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