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Transcriptional programs activated by exposure of human prostate cancer cells to androgen

Samuel E DePrimo16, Maximilian Diehn2, Joel B Nelson3, Robert E Reiter4, John Matese5, Mike Fero5, Robert Tibshirani6, Patrick O Brown7 and James D Brooks1*

Author Affiliations

1 Department of Urology, Room S 287, Stanford University School of Medicine, Stanford, CA 94305, USA

2 Department of Biochemistry and the Howard Hughes Medical Institute, Stanford University School of Medicine, Stanford, CA 94305, USA

3 Department of Urology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15232, USA

4 Department of Urology, UCLA School of Medicine, Los Angeles, CA 90095, USA

5 Department of Genetics, Stanford University School of Medicine, Stanford, CA 94305, USA

6 Department of Statistics, Stanford University School of Medicine, Stanford, CA 94305, USA

7 SUGEN, Inc., South San Francisco, CA 94080, USA

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Genome Biology 2002, 3:research0032-research0032.12  doi:10.1186/gb-2002-3-7-research0032

Published: 14 June 2002



Androgens are required for both normal prostate development and prostate carcinogenesis. We used DNA microarrays, representing approximately 18,000 genes, to examine the temporal program of gene expression following treatment of the human prostate cancer cell line LNCaP with a synthetic androgen.


We observed statistically significant changes in levels of transcripts of more than 500 genes. Many of these genes were previously reported androgen targets, but most were not previously known to be regulated by androgens. The androgen-induced expression programs in three additional androgen-responsive human prostate cancer cell lines, and in four androgen-independent subclones derived from LNCaP, shared many features with those observed in LNCaP, but some differences were observed. A remarkable fraction of the genes induced by androgen appeared to be related to production of seminal fluid and these genes included many with roles in protein folding, trafficking, and secretion.


Prostate cancer cell lines retain features of androgen responsiveness that reflect normal prostatic physiology. These results provide a broad view of the effect of androgen signaling on the transcriptional program in these cancer cells, and a foundation for further studies of androgen action.