ArticleMedicine2017
Microarray analysis of copy-number variations and gene expression profiles in prostate cancer.
Article in Medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 12 citations in OpenAlex.
- Research on the role and mechanism of FAT4 in the development and progression of tumor and non-tumor diseases.Discover oncology · 2026Review
- PCP4 inhibits the progression of prostate cancer through CaFrontiers in immunology · 2025Article
- Integrating single-cell and bulk RNA sequencing data unveils antigen presentation and process-related CAFS and establishes a predictive signature in prostate cancer.Journal of translational medicine · 2024Article
- Up-regulation of FAT4 enhances the chemosensitivity of colorectal cancer cells treated by 5-FU.Translational cancer research · 2020Article
- Structural variation at the CYP2C locus: Characterization of deletion and duplication alleles.Human mutation · 2019Article
- Transcriptional regulation of FoxM1 by HIF‑1α mediates hypoxia‑induced EMT in prostate cancer.Oncology reports · 2019Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThis study aimed to identify potential prostate cancer (PC)-related variations in gene expression profiles.
methodsMicroarray data from the GSE21032 dataset that contained the whole-transcript and exon-level expression profile (GSE21034) and Agilent 244K array-comparative genomic hybridization data (GSE21035) were downloaded from the Gene Expression Omnibus database. Differentially expressed genes (DEGs) and copy-number variations (CNVs) were identified between PC and normal tissue samples. Coexpression interactions of DEGs that contained CNVs (CNV-DEGs) were analyzed. Pathway enrichment analysis of CNV-DEGs was performed. Drugs targeting CNV-DEGs were searched using the Drug-Gene Interaction database.
resultsIn total, 679 DEGs were obtained, including 182 upregulated genes and 497 downregulated genes. A total of 48 amplified CNV regions and 45 deleted regions were determined. The number of CNVs at 8q and 8p was relatively higher in PC tissue. Only 16 DEGs, including 4 upregulated and 12 downregulated genes, showed a positive correlation with CNVs. In the coexpression network, 3 downregulated CNV-DEGs, including FAT4 (FAT atypical cadherin 4), PDE5A (phosphodiesterase 5A, cGMP-specific), and PCP4 (Purkinje cell protein 4), had a higher degree, and were enriched in specific pathways such as the calmodulin signaling pathway. Five of the 16 CNV-DEGs (e.g., PDE5A) were identified as drug targets.
conclusionThe identified CNV-DEGs could be implicated in the progression of human PC. The findings could lead to a better understanding of PC pathogenesis.
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