RESUMO
Background: Prostate adenocarcinoma is a frequent cancer among men with high incidence and mortality rates. Biomarkers are useful for the treatment of cancers, so we need to explore the regulatory network of prostate adenocarcinoma. Method: The database from University of California Santa Cruz was used to determine expression of messenger RNAs and microRNAs. Weighted correlation network analysis was used for classifying genes. Search Tool for Recurring Instances of Neighboring Genes and Cytoscape were used for the construction of PPI network and selection of hub genes. The microRNAs were predicted in miRactDB. The relations between microRNAs and messenger RNAs were assessed by Statistical Product and Service Solutions. The prognostic value was evaluated through Kaplan-Meier method. Kyoto Encyclopedia of Genes and Genomes, Gene Ontology and Gene Set Enrichment Analysis were used for predicting potential function. Results: 10 hub genes were all overexpressed in tumor tissues compared to normal tissues, but only aurora kinase B and nucleolar and spindle associated protein 1 were both significantly related to disease-free interval and progression-free interval time.Aurora kinase B and nucleolar and spindle associated protein 1 were negatively related to hsa-miR-1-3p, hsa-miR-133a-3p, hsa-miR-133b and hsa-miR-221-3p but positively related to hsa-miR-15b-5p, hsa-miR-21-5p, hsa-miR-106b-5p, hsa-miR-183-5p, hsa-miR-191-5p, hsa-miR-210-3p, hsa-miR-425-5p and hsa-miR-653-5p. All microRNAs except has-miR-653-5p significantly were related to the disease-free interval and progression-free interval time. The functions of microRNAs were enriched in cell cycle. Conclusion: We identified hub messenger RNAs and core microRNAs and established a novel messenger RNA-microRNA network associated with the prognosis of prostate adenocarcinoma.
RESUMO
BACKGROUND: Colon adenocarcinoma (COAD) is a highly heterogeneous disease, which is the second most common cancer in females and third in males. Collagen type I alpha 2 (COL1A2) has been documented to be involved in the carcinogenesis of multiple tumors; however, the expression and prognostic significance of COL1A2 and its underlying mechanism in COAD remains unclarified. MATERIALS AND METHODS: The general profile of COL1A2, its expression pattern, and prognostic value were systematically assessed through various bioinformatics tools. The protein level of COL1A2 was verified in COAD patients using immunohistochemistry analysis. In addition, enrichment analyses were performed to explore the possible regulatory pathways of COL1A2 in COAD. RESULTS: The mRNA and protein levels of COL1A2 were significantly increased in COAD than that in normal tissues (P < 0.05). The COL1A2 expression tended to increase along with cancer stages and nodal metastasis status in COAD, while the promoter methylation levels of COL1A2 might negatively related to its mRNA expression. Survival analysis showed that COL1A2 was a reliable predictor for distinguishing the status of disease-specific survival (DSS), overall survival (OS), and progression-free survival (PFS), and might serve as a robust independent prognostic biomarker for DSS and OS in COAD patients (P < 0.05). The enrichment analysis showed focal adhesion as the most possible regulatory pathway by COL1A2. CONCLUSION: Collectively, COL1A2 functioned as an independent prognostic biomarker and might be a potential therapeutic target in COAD.
