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[Cancer Research 64, 8867-8875, December 15, 2004]
© 2004 American Association for Cancer Research

Regular Articles

Androgen-Induced Differentiation and Tumorigenicity of Human Prostate Epithelial Cells

Raanan Berger1,6, Phillip G. Febbo1,4,6, Pradip K. Majumder1, Jean J. Zhao2, Shayan Mukherjee8, Sabina Signoretti5,7, K. Thirza Campbell1, William R. Sellers1,4,6,8, Thomas M. Roberts2,8, Massimo Loda5,7, Todd R. Golub3,8,9 and William C. Hahn1,4,6,7,8

Departments of 1 Medical Oncology, 2 Cancer Biology, and 3 Pediatric Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts; Departments of 4 Medicine and 5 Pathology, Brigham and Women’s Hospital, Boston, Massachusetts; Departments of 6 Medicine and 7 Pathology, Harvard Medical School, Boston, Massachusetts; and 8 Broad Institute of MIT and Harvard and 9 Howard Hughes Medical Institute, Cambridge, Massachusetts

Androgen ablation is the primary treatment modality for patients with metastatic prostate cancer; however, the role of androgen receptor signaling in prostate cancer development remains enigmatic. Using a series of genetically defined immortalized and tumorigenic human prostate epithelial cells, we found that introduction of the androgen receptor induced differentiation of transformed prostate epithelial cells to a luminal phenotype reminiscent of organ-confined prostate cancer when placed in the prostate microenvironment. Moreover, androgen receptor expression converted previously androgen-independent, tumorigenic prostate epithelial cells into cells dependent on testosterone for tumor formation. These observations indicate that androgen receptor expression is oncogenic and addictive for the human prostate epithelium.




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