Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

The transcriptional network for cell cycle regulation in prostate cancer

ABSTRACT: Several compounds were treated on the PC-3 cell line to investigate cell cycle regulation in prostate cancer through gene expression profile data. Our study demonstrated that several compounds induced cell cycle regulation in the CRPC (Castration-Resistant Prostate Cancer) cell model. Compounds (menthol, cineol, geraniol, icilin, linalool) were dissolved in ethanol as a vehicle at 0.1% working concentration and treated in PC-3 cells in triplicate. Vehicle-treated PC-3 cells in triplicate were used as a control.

ORGANISM(S): Homo sapiens

SUBMITTER: Ju-Hong Jeon

PROVIDER: E-GEOD-45567 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Icilin inhibits E2F1-mediated cell cycle regulatory programs in prostate cancer.

Lee Sanghoon S Chun Jung Nyeo JN Kim Su-Hwa SH So Insuk I Jeon Ju-Hong JH

Biochemical and biophysical research communications 20131112 4

Aberrant expression of cell cycle regulators have been implicated in prostate cancer development and progression. Therefore, understanding transcriptional networks controlling the cell cycle remain a challenge in the development of prostate cancer treatment. In this study, we found that icilin, a super-cooling agent, down-regulated the expression of cell cycle signature genes and caused G1 arrest in PC-3 prostate cancer cells. With reverse-engineering and an unbiased interrogation of a prostate ...[more]

PMID: 24239550

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Project description:Background: Aldo-keto reductase (AKR) 1C family member 3 (AKR1C3), one of four identified human AKR enzymes, catalyzes steroid, prostaglandin, and xenobiotic metabolism. In the prostate, AKR1C3 is up-regulated in localized and advanced prostate adenocarcinoma, and is associated with prostate cancer (PCa) aggressiveness. Here we provide initial evidence for potential roles of AKR1C3 in PCa progression. Methods: Spatial distribution of AKR1C3 was analyzed using immunohistochemical staining in prostate adenocarcinoma tissue array. Human PCa PC-3 cells were stably transfected with AKR1C3 cDNA to establish PC3-AKR1C3 transfectants. Microarray and bioinformatics analyses were performed to identify pathways that are activated by elevated AKR1C3 expression in PCa cells. Functional confirmation of microarray and bioinformatics results was performed by immunoblot analysis and an in vitro Matrigel angiogenesis assay. Results: Elevated AKR1C3 expression was specifically limited to human prostate adenocarcinoma. Microarray and bioinformatics analysis suggested that elevated AKR1C3 expression in PC-3 cells modulates estradiol and androgen metabolism and activates insulin growth factor (IGF)-1 and Akt signaling pathways. Immunoblots confirmed that phosphorylated levels of IGF-1 receptor (IGF-1R) and Akt are significantly up-regulated in PC3-AKR1C3 as compared to mock transfectants. PC3-AKR1C3 transfectants promoted endothelial cell tube formation in Matrigel as compared to parental PC-3 cells and mock transfectants. Conclusion: Microarray and bioinformatics data followed by biological analyses suggest that elevated AKR1C3 expression in PC-3 cells promotes PCa angiogenesis and aggressiveness. These results suggest AKR1C3 can promote the aggressiveness of PCa through modulating estrogen and androgen metabolism with subsequent activation of growth factor IGF-1 and cytoplasmic Akt signaling pathways. Total RNA from mock- and ACR1C3 transfected PC-3 cells was isolated, with 2 or 3 biological replicates each. Gene expression data from AKR1C3 transfected PC-3 cells were compared with mock-transfected data.

Dataset Information

The transcriptional network for cell cycle regulation in prostate cancer

Publications

Icilin inhibits E2F1-mediated cell cycle regulatory programs in prostate cancer.

Similar Datasets

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