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Background and purpose: Gene chip is a nucleic acid sequence analysis method which is based on hybridization. It is a high-through put assay which can widely detect the level of gene expression in different tissues and cell types. This study aimed to compare and bioinformatically analyze differentially expressed genes between higher malignant degree of prostate cancer tissues and prostate inflammation tissues. Methods: The total RNAs were isolated from tissues of prostate cancer and prostate inflammation by TRIzol method and then purified, reversely tran-scribed to cDNA with incorporating biotin labeling probe, hybridized with Affymetrix Human U133 Plus 2.0 (covering 47000 transcripts,representing 38500 distinct genes). Picture signals of fluorescence in gene array were scanned and differential expression of gene in two tissues were compared by Command Console Software 4.0. These differential expressed genes were analyzed by bioinformatics methods finally. Results: According to the fold change ≥2, P<0.05, 1819 differential expression genes including 1025 up-regulated genes and 794 down-regulated genes were discovered. GO enrichment analysis displayed that these differentially expressed genes were mainly involved in cell cycle, cell metabolism, etc. KEGG pathway analysis found that these genes were mainly involved in some metabolism pathways including purine nucleotide metabolism. The interactions between the proteins encoded by these genes were analyzed by STING. Twenty key nodes genes including TPX2, ANLN, NUSAP1, MELK, DLGAP5, KIF11, TOP2A, RRM2 were dis-covered. Then this study revealed CEP55 and ANLN might be related to the occurrence and metastasis of prostate cancer by looking through literature. Conclusion: During the development of prostate cancer, the activation of genes related to cell cycle and cell migration, the abnormalities of genes related to metabolism and the inhibition of genes related to cell adhesion play critical roles in the development of prostate cancer. CEP55 and ANLN were related to the occurrence and prognosis of prostate cancer by systematic analysis which provided a valuable clue for the next experiment.
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Background and purpose:Hypermethylated in cancer 1 (HIC1) is silenced in multiple cancer cells and tissues by DNA methylation of epigenetic modification, which may modulate the initiation and progression of tumors. However, there are few reports about this phenomenon in prostate cancer. This study aimed to investigate the status of HIC1 promoter methylation in prostate cancer using methylation methods.Methods:Methylation-specific polymerase chain reaction (MSP) and bisulfate sequencing PCR (BSP) were used to detect the methylation status ofHIC1 promoter in prostate cancer cell lines PC3 and C4-2B, prostate normal cell line PrEC, primary Chinese PCa tissues and the respective healthy control cases.HIC1 expression level was respectively determined by reverse transcription-PCR (RT-PCR) and Western blot assays in PC3, C4-2B and PrEC cells treated with 5-Aza-CdR.Results:We found that the percentages of HIC1 promoter methylation were 78.23%, 72.15% and 10.63% in PC3, C4-2B and PrEC cells by MSP analyses. Moreover, the levels of methylatedHIC1 promoter in 36 primary Chinese PCa tissues compared with the respective healthy control cases were 80.30%vs 31.56%. Expressions ofHIC1 mRNA and protein level were restored in PC3 and C4-2B cells after 5-Aza-CdR treatment.Conclusion:These findings demonstrate thatHIC1 promoter region is hypermethylated in prostate cancer, which results in silence or downregulation ofHIC1. The status ofHIC1 methylation can be a valuable marker in the early stage of prostate cancer and a potential therapeutic target.