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(American Journal of Pathology. 2002;161:1467-1474.)
© 2002 American Society for Investigative Pathology

Regular Articles

Heterogeneous Expression and Functions of Androgen Receptor Co-Factors in Primary Prostate Cancer

Peng Li*, Xin Yu{dagger}, Kai Ge{dagger}, Jonathan Melamed*, Robert G. Roeder{dagger} and Zhengxin Wang{ddagger}

From the Department of Pathology,* New York University Medical Center, New York, New York; the Laboratory of Biochemistry and Molecular Biology,{dagger} Rockefeller University, New York, New York; and the Department of Cancer Biology,{ddagger} University of Texas, MD Anderson Cancer Center, Houston, Texas

The androgen receptor (AR), a ligand-activated transcription factor of the steroid receptor superfamily, plays an important role in normal prostate growth and in prostate cancer. The recent identification of various AR co-factors prompted us to evaluate their possible roles in prostate tumorigenesis. To this end, we analyzed the expression of AR and eight of its co-factors by quantitative in situ RNA hybridization in 43 primary prostate cancers with different degrees of differentiation. Our results revealed nearly constant expression of AR and heterogeneous expression of AR co-factors, with increased expression of PIAS1 and Ran/ARA24, decreased expression of ELE1/ARA70, and no change in TMF1/ARA160, ARA54, SRC1, or TRAP220. Interestingly, whereas TMF1/ARA160, ELE1/ARA70, ARA54, RAN/ARA24, and PIAS1 were preferentially expressed in epithelial cells, another co-factor, ARA55, was preferentially expressed in stromal cells. Although the changes in levels of these co-activators did not correlate with Gleason score, their occurrence in high-grade prostatic intraepithelial neoplasia, suggests their involvement in initiation (or an early stage) of cancer. In addition, human prostate tumor cell proliferation and colony formation were markedly reduced by ELE1/ATRA70. Together, these findings indicate that changes in levels of expression of AR co-factors may play important, yet different, roles in prostate tumorigenesis.




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