Growing studies have implicated the association of ubiquitination-related genes (UbRGs) with the cancer progression and the long-term survival of patients. However, the prognostic values of UbRGs in lung adenocarcinoma (LUAD) have not been investigated. Our study aimed to establish a ubiquitination-related model for prognosis prediction and internal mechanism investigation. The transcriptome expression profiles and corresponding clinical information of LUAD were obtained from TCGA and GEO datasets. Differentially expressed genes (DEGs) were screened between LUAD specimens and nontumor specimens. Kaplan–Meier analysis and univariate assays were carried out on DEGs to preliminarily screen survival-related UbRGs. Then, the LASSO Cox regression model was applied to develop a multigene signature, which was then demonstrated in two GEO datasets by the use of Kaplan-Meier, ROC, and Cox analyses. We estimated the immune cell infiltration in tumor microenvironment via CIBERSORT and immunotherapy response through the TIDE algorithm. In this study, a total of 71 ubiquitination-related DEGs were identified. Nine UbRGs, including TUBA4A, TRIM2, PLK1, ARRB1, TRIM58, PLK1, ARRB1, CCNB1, TRIM6, PTTG1, and CCT2, were included to establish a risk model, which was validated in TCGA and GEO datasets. The multivariate assays demonstrated that the 9-UbRGs signature was a robust independent prognostic factor in the overall survival of LUAD patients. The abundance of CD8 T cells, activated CD4 T memory cells, resting NK cells and macrophages was higher in the high-risk group, and the TMB of high-risk group was statistically higher than the low-risk group. Multiple drugs approved by FAD, targeting UbRGs, were available for the treatment of LUAD. Overall, we identified a nine ubiquitination-related gene signature, and the signature may be applied to be a potential biomarker for CD8 T cells response and clinical responses to immune checkpoint inhibitors for LUAD.
Although many studies have investigated the association of single nucleotide polymorphisms (SNPs) in transforming growth factor beta1 (TGF-β1) gene with pulmonary fibrosis (PF), but their association is still controversial. To clarify this, we performed a meta-analysis.Studies related to TGF-β1 and PF were retrieved from PubMed, Medline, Embase, Scopus, and Wanfang (up to November 30, 2017). We targeted TGF-β1 SNPs that have been reported by ≥3 studies to be included in the current meta-analysis, resulting in only 1 final SNP (rs1800470). The odds ratios (ORs) and 95% confidence intervals (CIs) were estimated in the models of allele comparison (T vs C), homozygote comparison (TT vs CC), dominant (TT vs TC + CC), recessive (TT + TC vs CC) to evaluate the strength of the associations.A total of 7 case-control studies were included in this meta-analysis. Overall, no significant association between TGF-β1 rs1800470 and PF was found (T vs C: OR [95% CI] = 0.96 [0.80, 1.15]; TT vs CC: 0.87 [0.61, 1.22]; TT vs TC + CC: 0.80 [0.62, 1.04]; TT + TC vs CC: 1.13 [0.83, 1.54]). In subgroup analyses by ethnicity or original disease, no statistically significant association between TGF-β1 rs1800470 polymorphisms and PF was demonstrated.This meta-analysis revealed that TGF-β1 rs1800470 polymorphism was not associated with susceptibility to PF development.
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