Gene expression down-regulation in CD90+ prostate tumor-associated stromal cells involves potential organ-specific genes

Abstract Background The prostate stroma is a key mediator of epithelial differentiation and development, and potentially plays a role in the initiation and progression of prostate cancer. The tumor-associated stroma is marked by increased expression of CD90/THY1. Isolation and characterization of these stromal cells could provide valuable insight into the biology of the tumor microenvironment. Methods Prostate CD90+ stromal fibromuscular cells from tumor specimens were isolated by cell-sorting and analyzed by DNA microarray. Dataset analysis was used to compare gene expression between histologically normal and tumor-associated stromal cells. For comparison, stromal cells were also isolated and analyzed from the urinary bladder. Results The tumor-associated stromal cells were found to have decreased expression of genes involved in smooth muscle differentiation, and those detected in prostate but not bladder. Other differential expression between the stromal cell types included that of the CXC-chemokine genes. Conclusion CD90+ prostate tumor-associated stromal cells differed from their normal counterpart in expression of multiple genes, some of which are potentially involved in organ development.

We are grateful to Dr. Paul Lange and Dr. William Ellis for providing tissue for this study. We thank Adam Van Mason for collecting and preparing tissue specimens for our experiments. This work was supported by grants DK63630 from NIDDK and CA111244 from NCI. Its contents are solely the responsibility of the authors and do not necessarily represent the official views of the NIH. Additional funding supported RZNV from grant PM50 GMO76547/Center for Systems Biology and YAG from Department of Defense grant W81XWH-06-1-0108.

We are grateful to Dr. Paul Lange and Dr. William Ellis for providing tissue for this study. We thank Adam Van Mason for collecting and preparing tissue specimens for our experiments. This work was supported by grants DK63630 from NIDDK and CA111244 from NCI. Its contents are solely the responsibility of the authors and do not necessarily represent the official views of the NIH. Additional funding supported RZNV from grant PM50 GMO76547/Center for Systems Biology and YAG from Department of Defense grant W81XWH0610108.