SHIAN-YING SUNG2026-10-162026-10-162010-01-01Pure ID: 15209848Pure UUID: 11a4b1e7-ccd0-4567-b7d4-f286bb5633f410.1155/2010/232831https://www.scopus.com/pages/publications/77956811470https://scholars.csmu.edu.tw/handle/123456789/25065HS-27a human bone stromal cells, in 2D or 3D coultures, induced cellular plasticity in human prostate cancer ARCaP E and ARCaP M cells in an EMT model. Cocultured ARCaP E or ARCaP M cells with HS-27a, developed increased colony forming capacity and growth advantage, with ARCaP 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 in ARCaP E cells compared to ARCaP 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 both ARCaP E - and ARCaP 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.enjournal article