ObjectiveTo understand the molecular mechanisms underlying the carcinogenesis and progression of papillary thyroid carcinoma (PTC), and provide candidate targets for diagnosis and treatment of PTC.MethodsTo identify the differentially expressed genes (DEGs) in the carcinogenesis and progression of PTC, the study was carried by analyzing the microarray datasets downloaded from gene expression omnibus (GEO) database, and making a series of studies including the protein-protein interaction network, KEGG and GO enrichment analyses of DEGs.ResultsA total of 339 DEGs and 10 hub genes were identified. While the expression of KIT was downregulated in the samples of PTC, the figures for FN1, CCND1, TIMP1, ICAM1, APOE, MET, RUNX2, KRT19 and SERPINA1 were upregulated. After the hypothesis test was corrected by multiple tests, the results showed that the changes of APOE [false discovery rate (FDR)=0.047 5] and KIT (FDR=0.042 0) gene expression had a certain impact on recurrence free survival (RFS) of PTC patients, which was statistically significant.ConclusionsSurvival analysis showed that FN1, ICAM1, APOE, MET, KRT19, KIT and SERPINA1 may be involved in the carcinogenesis or prognosis of PTC. However, further studies are needed to elucidate the biological function of these genes in PTC.
ObjectiveTo evaluate the changes in the expression and significance of serum exosomal miRNAs in patients with DeBakey typeⅠacute aortic dissection (AAD). MethodsTwelve male patients with AAD and six healthy male medical examiners from our hospital were retrospectively included in this study. According to the time of chest pain, the AAD patients were divided into an AAD group within 24 h of chest pain onset, aged 47.00±8.79 years and an AAD group within 48 h of chest pain onset, aged 50.17±9.99 years. The healthy males were allocated to a control group, aged 49.17±4.26 years. Serum exosomal miRNAs were isolated, identified and quantified, and then differentially expressed exosomal miRNAs were screened. The bioinformatic analyses such as GO and KEGG were performed on the differentially expressed exosomal miRNAs. ResultsHigh-throughput screening results revealed differential expression of AAD serum exosomal miRNAs. The upregulated miRNAs of AAD groups was hsa-miR-574-5p (P<0.05), and downregulated miRNAs were hsa-miR-223-3p, hsa-miR-146b-5p, hsa-miR-15b-5p, and hsa-miR-155-5p (P<0.05). Further bioinformatic analysis of the above miRNAs revealed that they were mainly enriched in signaling pathways such as transforming growth factor-β, cell cycle and endoplasmic reticulum protein synthesis. ConclusionDifferential expressions of serum exosomal miRNAs in AAD patients may be related to the pathogenesis of AAD, providing new ideas and clues for further exploration of AAD diagnostic markers and pathogenesis.
Objective To explore the correlation and mechanism of ferroptosis with pulmonary fibrosis. Methods Pulmonary fibrosis tissue sequencing data were obtained from Gene Expression Omnibus and FerrDb databases from January 2019 to December 2023. Differentially expressed genes (DEGs) between the normal control group and the pulmonary fibrosis group were analyzed by bioinformatic method, and DEGs related to pulmonary iron addiction were extracted. The hub genes were screened by enrichment analysis, protein-protein interaction (PPI) analysis and random forest algorithm. The mouse model of pulmonary fibrosis was made for exercise intervention, and the expression of hub genes was verified by real-time quantitative reverse transcription polymerase chain reaction. Results A comparison of 103 patients with idiopathic pulmonary fibrosis and 103 normal lung tissues showed that 13 up-regulated genes and 7 down-regulated genes were identified as ferroptosis-related DEGs. PPI results showed that there was an interaction between these ferroptosis-related genes. The Kyoto Encyclopedia of Genes and Genomes pathway enrichment and Genome Ontology enrichment analysis showed that ferroptosis-related genes were involved in organic anion transport, hypoxia response, oxygen level reduction response, hypoxia-inducible factor-1 signaling pathway, renal cell carcinoma, and arachidonic acid metabolic signaling pathway. Genes identified by PPI analysis and random forest algorithm included CAV1, NOS2, GDF15, HNF4A, and CDKN2A. Real-time fluorescence quantitative polymerase chain reaction results of mouse fibrotic lung tissue showed that compared with the exercise group, the mRNA levels of NOS2, PTGS2 and GDF15 were up-regulated and the mRNA levels of CAV1 and CDKN2A were down-regulated in the bleomycin group (P<0.05); compared with the bleomycin group, the expression of CAV1 and CDKN2A increased and the expression of NOS2, PTGS2 and GDF15 decreased in the bleomycin + exercise group (P<0.05). Conclusions Bioinformatic analysis identifies 20 potential genes associating with ferroptosis in pulmonary fibrosis. CAV1, NOS2, GDF15, and CDKN2A influence the development of pulmonary fibrosis by modulating ferroptosis. Treadmill training can reduce ferroptosis in fibrotic tissues, thereby reducing lung inflammation.