Identification of a methyltransferase-related long noncoding RNA signature as a novel prognosis biomarker for lung adenocarcinoma.

BACKGROUND: Lung adenocarcinoma (LUAD) accounts for a high proportion of tumor deaths globally, while methyltransferase-related lncRNAs in LUAD were poorly studied. METHODS: In our study, we focused on two distinct cohorts, TCGA-LUAD and GSE3021, to establish a signature of methyltransferase-related long non-coding RNAs (MeRlncRNAs) in LUAD. We employed univariate Cox and LASSO regression analyses as our main analytical tools. The GSE30219 cohort served as the validation cohort for our findings. Furthermore, to explore the differential pathway enrichments between groups stratified by risk, we utilized Gene Set Enrichment Analysis (GSEA). Additionally, single-sample GSEA (ssGSEA) was conducted to assess the immune infiltration landscape within each sample. Reverse transcription quantitative PCR (RT-qPCR) was also performed to verify the expression of prognostic lncRNAs in both clinically normal and LUAD samples. RESULTS: In LUAD, we identified a set of 32 MeRlncRNAs. We further narrowed our focus to six prognostic lncRNAs to develop gene signatures. The TCGA-LUAD cohort and GSE30219 were utilized to validate the risk score model derived from these signatures. Our analysis showed that the risk score served as an independent prognostic factor, linked to immune-related pathways. Additionally, the analysis of immune infiltration revealed that the immune landscape in high-risk groups was suppressed, which could contribute to poorer prognoses. We also constructed a regulatory network comprising 6 prognostic lncRNAs, 19 miRNAs, and 21 mRNAs. Confirmatory RT-qPCR results aligned with public database findings, verifying the expression of these prognostic lncRNAs in the samples. CONCLUSION: The prognostic gene signature of LUAD associated with MeRlncRNAs that we provided, may offer us a comprehensive picture of the prognosis prediction for LUAD patients.

Prognostic value of lncRNAs related to fatty acid metabolism in lung adenocarcinoma and their correlation with tumor microenvironment based on bioinformatics analysis.

Background: As a key regulator of metabolic pathways, long non-coding RNA (lncRNA) has received much attention for its relationship with reprogrammed fatty acid metabolism (FAM). This study aimed to investigate the role of the FAM-related lncRNAs in the prognostic management of patients with lung adenocarcinoma (LUAD) using bioinformatics analysis techniques. Methods: We obtained LUAD-related transcriptomic data and clinical information from The Cancer Genome Atlas (TCGA) database. The lncRNA risk models associated with FMA were constructed by single-sample gene set enrichment analysis (ssGSEA), weighted gene co-expression network (WGCNA), differential expression analysis, overlap analysis, and Cox regression analysis. Kaplan-Meier (K-M) and receiver operating characteristic (ROC) curves were utilized to assess the predictive validity of the risk model. Gene set variation analysis (GSVA) revealed molecular mechanisms associated with the risk model. ssGSEA and microenvironment cell populations-counter (MCP-counter) demonstrated the immune landscape of LUAD patients. The relationships between lncRNAs, miRNAs, and mRNAs were predicted by using LncBase v.2 and miRTarBase. The lncRNA-miRNA-mRNA regulatory network was visualized with Cytoscape v3.4.0. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis was performed using DAVID v6.8. Quantitative real-time fluorescence PCR (qRT-PCR) was performed to verify the expression levels of the prognostic lncRNAs. Results: We identified 249 differentially expressed FMA-related lncRNAs in TCGA-LUAD, six of which were used to construct a risk model with appreciable predictive power. GSVA results suggested that the risk model may be involved in regulating fatty acid synthesis/metabolism, gene repair, and immune/inflammatory responses in the LUAD process. Immune landscape analysis demonstrated a lower abundance of immune cells in the high-risk group of patients associated with poor prognosis. Moreover, we predicted 279 competing endogenous RNA (ceRNA) mechanisms for 6 prognostic lncRNAs with 39 miRNAs and 201 mRNAs. Functional enrichment analysis indicated that the ceRNA network may be involved in the process of LUAD by participating in genomic transcription, influencing the cell cycle, and regulating tissue and organogenesis. In vitro experiments showed that prognostic lncRNA CTA-384D8.35, lncRNA RP5-1059L7.1, and lncRNA Z83851.4 were significantly upregulated in LUAD primary tumor tissues, while lncRNA RP11-401P9.4, lncRNA CTA-384D8.35, and lncRNA RP11-259K15.2 were expressed at higher levels in paraneoplastic tissues. Conclusion: In summary, the prognostic factors identified in this study can be used as potential biomarkers for clinical applications. ceRNA network construction provides a new vision for the study of LUAD pathogenesis.

Extensive Arch Repair with a Novel Two-Branched Stent Graft in Acute Type A Aortic Dissection.

PURPOSE: In this study, we compared the early results between the extensive arch repair with a novel two-branched stent graft (TSG) and the traditional technique. METHODS: Between 2013 July and 2015 March, 63 acute type A aortic dissection (ATAAD) patients from four cardiac centers with indications for extensive arch repair were included in this study. Finally, 28 patients were involved in the traditional procedure (TP) group (23 males with the age of 49.75 ± 9.26 years) and 35 patients were involved in the TSG group (29 males with the age of 53.82 ± 8.17 years). RESULTS: The operation was successful in all patients. The selective cerebral perfusion time, total operation time, and chest drainage within 24 hours after the operation in the TSG group were significantly less than those in the TP group (P ≤0.05). The mean follow-up time was 11.17 ± 1.74 months in the TP group and 11.94 ± 4.29 months in the TSG group. No statistical differences were found in aortic diameter, false lumen diameter, and true lumen diameter at the diaphragmatic level during the follow-up. CONCLUSION: Our technique with a novel TSG simplified the extensive arch repair procedure and was an effective way for the treatment of ATAAD.