Tumor-stromal interactions influence radiation sensitivity in epithelial- versus mesenchymal-like prostate cancer cells

Clayton Yates, Sajni Josson, Starlette Sharp, Shian Ying Sung, Peter A S Johnstone, Ritu Aneja, Ruoxiang Wang, Murali Gururajan, Timothy Turner, Leland W K Chung

Research output: Contribution to journalArticle

27 Citations (Scopus)

Abstract

HS-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.

Original languageEnglish
Article number232831
JournalJournal of Oncology
DOIs
Publication statusPublished - 2010
Externally publishedYes

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Radiation Tolerance
Prostatic Neoplasms
Neoplasms
Cadherins
Stromal Cells
Integrin alpha Chains
Bone and Bones
Radiation
Prostate
Blocking Antibodies
Cell Adhesion Molecules
Mesenchymal Stromal Cells
Cell Survival
Epithelial Cells
Antibodies
Growth

ASJC Scopus subject areas

  • Oncology

Cite this

Tumor-stromal interactions influence radiation sensitivity in epithelial- versus mesenchymal-like prostate cancer cells. / Yates, Clayton; Josson, Sajni; Sharp, Starlette; Sung, Shian Ying; Johnstone, Peter A S; Aneja, Ritu; Wang, Ruoxiang; Gururajan, Murali; Turner, Timothy; Chung, Leland W K.

In: Journal of Oncology, 2010.

Research output: Contribution to journalArticle

Yates, Clayton ; Josson, Sajni ; Sharp, Starlette ; Sung, Shian Ying ; Johnstone, Peter A S ; Aneja, Ritu ; Wang, Ruoxiang ; Gururajan, Murali ; Turner, Timothy ; Chung, Leland W K. / Tumor-stromal interactions influence radiation sensitivity in epithelial- versus mesenchymal-like prostate cancer cells. In: Journal of Oncology. 2010.
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abstract = "HS-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.",
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AU - Josson, Sajni

AU - Sharp, Starlette

AU - Sung, Shian Ying

AU - Johnstone, Peter A S

AU - Aneja, Ritu

AU - Wang, Ruoxiang

AU - Gururajan, Murali

AU - Turner, Timothy

AU - Chung, Leland W K

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