Background/Aims: Whether the level of long noncoding RNA plasmacytoma variant translocation 1 gene (lncRNA PVT1) expression influences the clinical development and outcome of human cancers has not been thoroughly elucidated to date. Inconsistencies still exist regarding the associations between PVT1 and the clinicopathological features, including patient survival data. Additionally, the regulatory mechanism of PVT1 among human cancers remains unclear. Methods: we conducted a comprehensive inquiry to verify the implication of PVT1 expression in cancer patients by conducting a meta-analysis of 19 selected studies and The Cancer Genome Atlas (TCGA) database to examine the relationship between PVT1 expression and both the prognosis and clinicopathological features of cancer patients using STATA 12.0. In addition, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses of the potential mRNA target genes of PVT1 gathered from TANRIC and Multi Experiment Matrix (MEM) were performed. Results: The level of PVT1 expression in tumor tissues was higher than in paired non-cancer tissues and was significantly associated with a poorer prognosis in cancer patients. Additionally, overexpression of PVT1 was significantly correlated with histological differentiation, tumor (T) classification, lymph node (N) classification and TNM stages. Furthermore, a total of 462 validated target genes were identified, and the GO and KEGG analyses demonstrated that the validated targets of PVT1 were significantly enriched in several pathways, including the GnRH signaling pathway, the Cytokine-cytokine receptor interaction pathway, the Inflammatory mediator regulation of TRP channels pathway, and the Neuroactive ligand-receptor interaction pathway. Conclusion: PVT1 may serve as a potential biomarker associated with the progression and prognosis of human cancers.
Previous studies demonstrated that miRNA-1 (miR-1) is downregulated in certain human cancer and serves a crucial role in the progression of cancer. However, there are only a few previous studies examining the association between miR-1 and lung squamous cell carcinoma (LUSC) and the regulatory mechanism of miR-1 in LUSC remains unclear. Therefore, the present study investigated the clinical significance and determined the potential molecular mechanism of miR-1 in LUSC. The expression of miR-1 and its clinical significance in LUSC was examined by conducting a meta-analysis of 12 studies using Stata 14, MetaDiSc1.4 and SPSS version 23. In addition, Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses were performed using the potential target genes of miR-1 gathered from Gene Expression Omnibus and ArrayExpress. Meta-analysis demonstrated that miR-1 was significantly downregulated in LUSC [standardized mean difference: −1.44; 95% confidence interval (CI): −2.08, −0.81], and the area under the curve was 0.9096 (Q*=0.8416) with sensitivity of 0.71 (95% CI: 0.66, 0.76) and specificity of 0.88 (95% CI: 0.86, 0.90). The pooled positive likelihood ratio and negative likelihood ratio were 4.93 (95% CI: 2.54, 9.55) and 0.24 (95% CI: 0.10, 0.54), respectively. Bioinformatics analysis demonstrated that miR-1 may be involved in the progression of LUSC via the ‘cell cycle’, ‘p53 signaling pathway’, ‘Fanconi anemia pathway’, ‘homologous recombination’, ‘glycine, serine and threonine metabolism’ and ‘oocyte meiosis’. In summary, miR-1 was significantly downregulated in LUSC, suggesting a novel and promising non-invasive biomarker for diagnosing LUSC, and miR-1 was involved in LUSC progression via a number of significant pathways.
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