Tumor-Stromal Interactions Influence Radiation Sensitivity in Epithelial- versus Mesenchymal-Like Prostate Cancer Cells. (27th June 2010)

• Record Type: Journal Article
• Authors: Josson, Sajni; Sharp, Starlette; Sung, Shian-Ying; Johnstone, Peter A. S.; Aneja, Ritu; Wang, Ruoxiang; Gururajan, Murali; Turner, Timothy; Chung, Leland W. K.; Yates, Clayton
• Other Names: Andl Claudia D. Academic Editor.
• Is Part Of: Journal of oncology. Volume 2010(2010)
• Publication Date: 2010-06-27
• Subjects: Oncology -- Research -- Periodicals; Tumors -- Periodicals; Neoplasms; Oncology -- Research; Tumors; Periodicals; Periodicals; 616.994
• DOI: 10.1155/2010/232831
• Languages: English
• ISSNs: 1687-8450

Abstract

Abstract : HS-27a human bone stromal cells, in 2D or 3D coultures, induced cellular plasticity in human prostate cancerARCaP E andARCaP M cells in an EMT model. CoculturedARCaP E orARCaP M cells with HS-27a, developed increased colony forming capacity and growth advantage, withARCaP E 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 inARCaP E cells compared toARCaP M 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 bothARCaP E - andARCaP M -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.