Abstract LB-190: Soluble E-Cadherin promotes cell invasion but not proliferation in prostate cancer

Abstract

Abstract Metastasis is responsible for the majority of prostate cancer-related deaths. Despite progress in early detection and management, there remains no effective, long-term cure for metastatic prostate cancer, partially due to the unclear molecular mechanism of cancer cell invasion and metastasis. Clinical reports discovered that soluble E-cadherin (sE-Cad, the cleaved ectodomain of human E-Cadherin protein) was elevated in body fluids and serum of patients with a variety of cancers, and its serum levels have been shown to correlate positively with metastatic cancers and disease invasiveness. However, little is known about the role of sE-Cad in metastasis, or the molecular mechanism of its abnormal accumulation in cancerous microenvironment. Our lab generated C4-2 prostate cancer cell lines which would secret synthetic sE-Cad by Doxycycline induction. We found that increased sE-Cad in the conditioned medium promotes cell invasion, but not cell proliferation. We analyzed the protein subcellular localizations in different cell compartments (membrane, cytoskeleton, nucleus and cytoplasm) and observed increased binding of synthetic sE-Cad to membrane E-Cadherin, indicating that sE-Cad could promote cell motility by interacting with membrane proteins and possibly disrupting the cell-cell adhesion. This work is supported by Wake Forest University institutional funds to KC Balaji and by NIH grant CA079448 to X Fang. Citation Format: Xiaolan Fang, K. C. Balaji, Bita NickKholgh, Kenneth Gyabaah. Soluble E-Cadherin promotes cell invasion but not proliferation in prostate cancer. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr LB-190. doi:10.1158/1538-7445.AM2014-LB-190