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Sex-Determining Region Y Box 4 Is a Transforming Oncogene in Human Prostate Cancer Cells

¹ Department of Pathology and Laboratory Medicine and ² Winship Cancer Institute, Emory University School of Medicine and Programs in ³ Genetics and Molecular Biology and ⁴ Biochemistry, Cell, and Developmental Biology, Emory University, Atlanta, Georgia

Requests for reprints: Carlos S. Moreno, Department of Pathology and Laboratory Medicine, Winship Cancer Institute, Emory University School of Medicine, Whitehead Research Building, Room 105J, 615 Michael Street, Atlanta, GA 30322. Phone: 404-712-2809; Fax: 404-727-8538; E-mail: cmoreno{at}emory.edu.

Prostate cancer is the most commonly diagnosed noncutaneous neoplasm and second most common cause of cancer-related mortality in western men. To investigate the mechanisms of prostate cancer development and progression, we did expression profiling of human prostate cancer and benign tissues. We show that the SOX4 is overexpressed in prostate tumor samples compared with benign tissues by microarray analysis, real-time PCR, and immunohistochemistry. We also show that SOX4 expression is highly correlated with Gleason score at the mRNA and protein level using tissue microarrays. Genes affected by SOX4 expression were also identified, including BCL10, CSF1, and NcoA4/ARA70. TLE-1 and BBC3/PUMA were identified as direct targets of SOX4. Silencing of SOX4 by small interfering RNA transfection induced apoptosis of prostate cancer cells, suggesting that SOX4 could be a therapeutic target for prostate cancer. Stable transfection of SOX4 into nontransformed prostate cells enabled colony formation in soft agar, suggesting that, in the proper cellular context, SOX4 can be a transforming oncogene. (Cancer Res 2006; 66(8): 4011-9)

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