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Journal of Oncology
Volume 2010 (2010), Article ID 232831, 10 pages
Research Article

Tumor-Stromal Interactions Influence Radiation Sensitivity in Epithelial- versus Mesenchymal-Like Prostate Cancer Cells

1Department of Urology, Emory School of Medicine, Atlanta, GA 30311, USA
2Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA
3Department of Biology and Center for Cancer Research, Tuskegee University, Carver Research Foundation, Tuskegee, AL 36088, USA
4Department of Radiation Oncology, Emory School of Medicine, Atlanta, GA 30322, USA
5Department of Biology, Georgia State University, Atlanta, GA 30303, USA

Received 15 March 2010; Revised 12 May 2010; Accepted 12 May 2010

Academic Editor: Claudia D. Andl

Copyright © 2010 Sajni Josson et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


HS-27a human bone stromal cells, in 2D or 3D coultures, induced cellular plasticity in human prostate cancer and cells in an EMT model. Cocultured or cells with HS-27a, developed increased colony forming capacity and growth advantage, with exhibiting the most significant increases in presence of bone or prostate stroma cells. Prostate (Pt-N or Pt-C) or bone (HS-27a) stromal cells induced significant resistance to radiation treatment in cells compared to cells. However pretreatment with anti-E-cadherin antibody (SHEP8-7) or anti-alpha v integrin blocking antibody (CNT095) significantly decreased stromal cell-induced radiation resistance in both - and -cocultured cells. Taken together the data suggest that mesenchymal-like cancer cells reverting to epithelial-like cells in the bone microenvironment through interaction with bone marrow stromal cells and reexpress E-cadherin. These cell adhesion molecules such as E-cadherin and integrin alpha v in cancer cells induce cell survival signals and mediate resistance to cancer treatments such as radiation.