Journal Article

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

Dev Karan, David L. Kelly, Angie Rizzino, Ming-Fong Lin and Surinder K. Batra

in Carcinogenesis

Volume 23, issue 6, pages 967-976
Published in print June 2002 | ISSN: 0143-3334
Published online June 2002 | e-ISSN: 1460-2180 | DOI: http://dx.doi.org/10.1093/carcin/23.6.967
Expression profile of differentially-regulated genes during progression of androgen-independent growth in human prostate cancer cells

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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, α-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.

Keywords: CCNH, cyclin H; CDK-2, cyclin dependent kinase-2; LDH-A, lactate dehydrogenase-A; MIC-1, macrophage inhibitory cytokine-1; MIF, macrophage migration inhibitory factor; NBP, guanine nucleotide-binding protein Gi, alpha-1 subunit; PSA, prostate-specific antigen; PSM, prostate-specific membrane antigen; PuF, purine-binding transcription factor; RPL10, 60S ribosomal protein L32, RPS16, 40S ribosomal protein S16.

Journal Article.  6161 words.  Illustrated.

Subjects: Clinical Cytogenetics and Molecular Genetics

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