Yong Cao

Background: The patients of non–small cell lung cancer (NSCLC) with malignant pleural effusion (MPE) typically had poor prognosis. It was still challenging to predict overall survival (OS) and make reasonable clinical treatment. Methods: Patients diagnosed with NSCLC and MPE between January 2018 and January 2023 at Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, were retrospectively identified. The cohort was randomly divided into the training and validation groups. Propensity score matching was performed, followed by COX regression analysis based on the matched patients. A nomogram was constructed based on the multivariate COX regression results. The performance of the nomogram was evaluated using calibration and concordance indices, as well as receiver operating characteristic curves. Results: A total of 306 patients were included in this study. The median OS for the entire cohort was 233 days (95% confidence interval, 168.68–297.33), which improved to 242 days (95% confidence interval, 158.28–325.72) post–propensity score matching. Independent risk factors affecting OS included a history of respiratory system diseases, leukocyte count, neutrophil-to-lymphocyte ratio, serum albumin level, and targeted therapy. A nomogram predicting OS was developed based on the COX multivariate regression analysis. The concordance indices for these nomograms were 0.732 and 0.747 for the training and validation cohorts, respectively. Calibration curves demonstrated a good alignment between the predicted and actual survival probabilities at various time points in both cohorts. Conclusions: The nomogram was successfully constructed to predict OS at 6 months, 1 year, and 2 years for NSCLC patients with MPE. This nomogram can potentially aid in clinical decision-making regarding the benefits of targeted therapy in this patient population.

Gastric cancer is one of the most common types of carcinoma with a threat to global health. MicroRNA-760 (miR-760) was significantly down-regulated in the primary tumour of patients with advanced gastric cancer. However, the role of miR-760 in gastric cancer is still unclear. Herein, miR-760 was down-regulated in gastric cancer tissues. Moreover, miR-760 overexpression and knockdown were conducted in gastric cancer cells (MGC-803 and SGC-7901) in vitro. The in vitro functional assays proved that miR-760 overexpression reduced cell viability, cell cycle, migration and invasion, promoted apoptosis and suppressed MMP activity in MGC-803 cells. Conversely, miR-760 knockdown led to the opposite in SGC-7901 cells. Notably, bone marrow stromal antigen 2 (BST2) was verified as a target gene of miR-760. MiR-760 mimics down-regulated BST2 level in gastric cancer tissues and in MGC-803 cells, whereas miR-760 inhibitor up-regulated its level in SGC-7901 cells. MiR-760-regulated cell properties through reduction of BST2. In addition, miR-760 inhibited tumourigenesis in a nude mouse xenograft model in vivo. In conclusion, our results demonstrated that miR-760 exhibited a suppressive role in gastric cancer via inhibiting BST2, indicating that miR-760/BST2 axis may provide promising therapeutic target for gastric cancer.

Objective: The aim of the study was to determine the expression profile of long noncoding RNAs (lncRNAs) in CD4⁺ T cells from COPD patients and explore the clinical value of the lncRNAs. Methods: First, microarray analysis was performed. Differentially expressed lncRNAs were validated by quantitative real-time reverse transcription-PCR (qRT-PCR) in samples from 56 patients with acute exacerbations of COPD (AECOPD), 56 patients with stable COPD, and 35 healthy controls. Meanwhile, the clinical value was tested by receiver operating characteristic curve analysis. The functions of lncRNAs were analyzed by the Gene Ontology and Kyoto Encyclopedia of Genes and Genomes database. The potential target genes that might be regulated by NR-026690 and ENST00000447867 were identified by the lncRNA-mRNA network and competing endogenous RNA network. The transcriptional expression level of rap guanine nucleotide exchange factor 3 (RAPGEF3) was tested by qRT-PCR. The correlation of the expression between NR-026690, ENST00000447867, and RAPGEF3 was analyzed by Spearman’s correlation test. Results: We found that the relative expression levels of ENST00000447867 and NR-026690 in the CD4⁺ T cells of AECOPD patients were significantly higher than in the stable COPD patients and control subjects by microarray and qRT-PCR validation. The transcriptional expression level of RAPGEF3 in the CD4⁺ T cells was significantly higher in the AECOPD group compared to the control group (PPr=0.4925, Pr=0.4065, PConclusion: NR-026690 and ENST00000447867 might be potential biomarkers for COPD. They might affect RAPGEF3 as miRNA sponges to regulate COPD development.

Asthma is a chronic T helper type 2 (Th2) cell‑mediated inflammatory disease characterized by airway hyperresponsiveness (AHR) and airway inflammation. Although the majority of patients with asthma can achieve a good level of control with existing treatments, asthma runs a chronic course and the effectiveness of current treatment is not satisfactory for certain patients. MicroRNAs (miRNAs) are short noncoding RNAs that suppress gene expression at the post‑transcriptional level; their role in regulating allergic inflammation remains largely unknown. The present study aimed to explore the role of miRNA‑155 in the pathogenesis of asthma and its potential as a target for treatment. The expression of miRNA‑155 increased in ovalbumin‑sensitized and challenged mice compared with control mice, and lentiviral vector‑delivered small interfering (si)RNA targeting miRNA‑155 resulted in reduced AHR, airway inflammation and Th2 cytokine production. The data from the present study indicate that miRNA‑155 serves an important role in the pathogenesis of asthma, and that lentiviral vector‑delivered siRNA targeting miRNA‑155 may serve as a novel approach for the treatment of allergic asthma.