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Carcinogenesis, Vol. 23, No. 6, 967-976, June 2002
© 2002 Oxford University Press

CANCER BIOLOGY

Expression profile of differentially-regulated genes during progression of androgen-independent growth in human prostate cancer cells

Dev Karan1, David L. Kelly2, Angie Rizzino1,,2, Ming-Fong Lin1,,2,,3 and Surinder K. Batra1,,2,,4

1 Department of Biochemistry and Molecular Biology,
2 Eppley Institute for Research in Cancer and Allied Diseases and
3 Department of Surgery, Section of Urology, University of Nebraska Medical Center, Omaha, NE, USA

Because of the heterogeneous nature of prostate cancer, identifying the molecular mechanisms involved during the transition from an androgen-sensitive to an androgen-independent phenotype is very complex. An LNCaP cell model that recapitulates prostate cancer progression, comprising early passage androgen-sensitive (LNCaP-C33) and late passage androgen-independent (LNCaP-C81) phenotypes, would help to provide a better understanding of such molecular events. In this study, we examined the genes expressed by LNCaP-C33 and LNCaP-C81 cells using cDNA microarrays containing 1176 known genes. This analysis demonstrated that 34 genes are up-regulated and eight genes are down-regulated in androgen-independent cells. Northern blot analysis confirmed the differences identified by microarrays on several candidate genes, including c-MYC, c-MYC purine-binding transcription factor (PuF), macrophage migration inhibitory factor (MIF), macrophage inhibitory cytokine-1 (MIC-1), lactate dehydrogenase-A (LDH-A), guanine nucleotide-binding protein Gi, {alpha}-1 subunit (NBP), cyclin dependent kinase-2 (CDK-2), prostate-specific membrane antigen (PSM), cyclin H (CCNH), 60S ribosomal protein L10 (RPL10), 60S ribosomal protein L32 (RPL32), and 40S ribosomal protein S16 (RPS16). These differentially-regulated genes are correlated with progression of human prostate cancer and may be of therapeutic relevance as well as an aid in understanding the molecular genetic events involved in the development of this disease's hormone-refractory behavior.


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