Background To explore the role of non‐coding RNA activated by DNA damage (NORAD), a long non‐coding ribonucleic acid (lncRNA), in non‐small cell lung cancer (NSCLC) and its possible mechanism. Methods Quantitative real‐time polymerase chain reaction was adopted for the detection of the expression levels of NORAD, micro RNA (miR)‐656‐3p, and AKT serine/threonine kinase 1 (AKT1). The effects of NORAD, miR‐656‐3p, and AKT1 on cell proliferation and migration were examined through the Cell Counting Kit‐8 (CCK‐8) and Transwell assay. Subsequently, the binding relationships between miR‐656‐3p and AKT1 and between miR‐656‐3p and NORAD were verified by dual‐luciferase reporter gene assay. Finally, the potential mechanisms of action of NORAD and miR‐656‐3p were explored through the torsion experiment. Results The lncRNA NORAD expression level in NSCLC patients was notably higher than that in people in control group, that in patients with metastasis was higher than that in patients without metastasis, and that in patients with NSCLC in stage III‐IV was significantly higher than that in patients with NSCLC in stage I‐II. Elevation of NORAD stimulated the proliferation and migration of NSCLC A549/H460 cells. According to the reporter gene assay, NORAD could bind to miR‐656‐3p. Besides, miR‐656‐3p was significantly under‐expressed in cancer tissues of patients with NSCLC, and overexpression of miR‐656‐3p could block the proliferation and migration of A549/H460 cells and reversed promotion on cell proliferation and migration by NORAD. Furthermore, the reporter gene assay revealed that the overexpression of AKT1, a miR‐656‐3p target gene, could reverse miR‐656‐3p's inhibitory effect on the proliferation and migration of A549/H460 cells. Conclusion LncRNA NORAD is capable of promoting the proliferation and migration of NSCLC cells, and its mechanism may be that it increases the AKT1 expression by adsorbing miR‐656‐3p.
Background Comorbid congestive heart failure (CHF) was associated with worse prognosis in patients with chronic obstructive pulmonary disease (COPD), while few studies specially investigated critically ill patients. This study investigated the associations between comorbid COPD with or without CHF and prognosis of patients admitted to intensive care units (ICU). Methods We conducted a retrospective cohort study in the Medical Information Mart for Intensive Care III database. Adult ICU patients were included and categorized as patients without COPD and CHF, patients with COPD but without CHF, patients with CHF but without COPD, and patients with both COPD and CHF. The study outcomes were 28-day mortality and 90-day mortality after ICU admission. Kaplan–Meier curves were plotted to estimate the survival distributions between groups and multivariable Cox regression analyses were employed to evaluate the associations between comorbid COPD and/or CHF and the study outcomes. Results A total of 29,589 patients were included with 20,507 patients without COPD and CHF, 1575 patients with COPD, 6190 patients with CHF, and 1317 patients with both COPD and CHF. The highest 28-day mortality rate and 90-day mortality rate were found in patients with both COPD and CHF (15.95% and 25.74%, respectively), while patients with COPD and patients with CHF had similar mortality rates, also observed in Kaplan–Meier curves. Compared with patients without COPD or CHF, comorbid COPD or CHF both significantly increased the risk of 28-day mortality and 90-day mortality, but comorbid COPD and CHF together was associated with the highest risk of mortality (hazard ratio 1.55 (95% confidence interval (CI) 1.33–1.80) and 1.25 (95% CI 1.16–1.35) for 28-day mortality and 90-day mortality, respectively), while no significant interaction between COPD and CHF was found. Conclusion ICU patients with comorbid COPD or CHF both experienced greater mortalities, while these two risk factors seemed to play an independent role.
Objective. To screen CXC chemokines related to the risk of lung adenocarcinoma (LUAD) using bioinformatics and construct a CXC-based prognostic risk model to improve the diagnosis and treatment of LUAD patients. Methods. The Cancer Genome Atlas (TCGA) database and Gene Expression Omnibus (GEO) database were searched to obtain mRNA expression data and clinicopathological information of LUAD patients. CXC genes differentially expressed in LUAD were screened using the R packages. Further, risk factors significantly associated with the survival of LUAD patients were obtained by the univariate Cox proportional hazard regression, LASSO regression, and multivariate Cox proportional hazard regression analysis, following which a risk prediction model was constructed. The performance of the CXCL13-based model in predicting the prognosis of low-risk and high-risk effect LUAD patients was verified, and the association between the model and the degree of tumor immune cell infiltration was investigated. Results. CXCL13 was significantly highly expressed in the cancer tissues of LUAD patients. The risk of death in patients with highly expressed CXCL13 was about 1.5 times higher than in those with lowly expressed CXCL13 ( HR = 1.5153357 ). CXCL13-based risk scoring showed that the high-risk score of LUAD patients was significantly correlated with poor prognosis, but no relation between the two was found in the GEO validation sets, suggesting that this risk model may not be accurate enough. In addition, activated B cells, CD4+ T cells, CD8+ T cells, and dendritic cells were significantly positively correlated with the high risk of LUAD. Conclusions. Although we found that a high expression of CXCL13 was associated with a high risk of death and immune cell infiltration and activation in LUAD patients, the CXCL13-based risk model was not accurate enough for predicting the prognosis of LUAD patients.
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