Long noncoding RNAs (lncRNAs) reportedly play critical roles in the pathogenesis of various cancers, including lung adenocarcinoma (LUAD). However, the expression level, clinical significance, and potential function of lncRNA-AC092718.4 in LUAD remain unclear. In this study, we found that AC092718.4 was highly expressed in LUAD and high expression of AC092718.4 was correlated with poor overall survival (OS) and disease-specific survival (DSS) in LUAD. Cox regression analysis confirmed that AC092718.4 was an independent factor for LUAD prognosis. Kyoto Encyclopedia of Genes and Genomes (KEGG) results showed that AC092718.4 was involved in the PI3K-Akt signaling pathway, Th17 cell differentiation, and cell apoptosis. AC092718.4 expression was correlated with immune cell infiltration. Finally, we found that the knockdown of AC092718.4 inhibited lung adenocarcinoma (LUAD) cell growth and promote cell apoptosis. Our findings confirmed that AC092718.4 may serve as a potential prognostic biomarker in LUAD.

Objective. Bioinformatics methods were used to analyze non-small-cell lung cancer gene chip data, screen differentially expressed genes (DEGs), explore biomarkers related to NSCLC prognosis, provide new targets for the treatment of NSCLC, and build immunotyping and line-map model. Methods. NSCLC-related gene chip data were downloaded from the GEO database, and the common DEGs of the two datasets were screened by using the GEO2R tool and FunRich 3.1.3 software. DAVID database was used for GO analysis and KEGG analysis of DEGs, and protein-protein interaction (PPI) network was constructed by STRING database and Cytoscape 3.8.0 software, and the top 20 hub genes were analyzed and screened out. The expression of pivot genes and their relationship with prognosis were verified by multiple external databases. Results. 159 common DEGs were screened from the two datasets. PPI network was constructed and analyzed, and the genes with the top 20 connectivity were selected as the pivotal genes of this study. The results of survival analysis and the patients survival curve was reflected in the line graph model of NSCLC. Conclusion. Through the screening and identification of the VIM-AS1 gene, as well as the analysis of immune infiltration and immune typing, the successful establishment of the rosette model has a certain guiding value for the molecular targeted therapy of patients with non-small-cell lung cancer.

The prediction of long non-coding RNA (lncRNA) subcellular localization is essential to the understanding of its function and involvement in cellular regulation. Traditional biological experimental methods are costly and time-consuming, making computational methods the preferred approach for predicting lncRNA subcellular localization (LSL). However, existing computational methods have limitations due to the structural characteristics of lncRNAs and the uneven distribution of data across subcellular compartments. We propose a discrete wavelet transform (DWT)-based model for predicting LSL, called DlncRNALoc. We construct a physicochemical property matrix of a 2-tuple bases based on lncRNA sequences, and we introduce a DWT lncRNA feature extraction method. We use the Synthetic Minority Over-sampling Technique (SMOTE) for oversampling and the local fisher discriminant analysis (LFDA) algorithm to optimize feature information. The optimized feature vectors are fed into support vector machine (SVM) to construct a predictive model. DlncRNALoc has been applied for a five-fold cross-validation on the three sets of benchmark datasets. Extensive experiments have demonstrated the superiority and effectiveness of the DlncRNALoc model in predicting LSL.

Tissue-resident memory T cells (Trm) are a subset of memory T cells that establish residency in peripheral tissues and do not re-enter circulation under homeostasis, playing a central role in local immune responses. Recent studies have revealed that Trm cells play a dual role in immune protection and immunopathology: in the tumor microenvironment they can directly kill tumor cells and enhance the efficacy of immunotherapies, serving as key mediators of antitumor immunity; conversely, in autoimmune diseases they may persist long-term and drive chronic inflammation and tissue damage. This functional duality is closely linked to the microenvironmental signals, transcriptional programs, and metabolic states that shape Trm cells. This review systematically examines the developmental differentiation and molecular features of Trm cells, their bidirectional regulatory mechanisms in cancer and autoimmunity, and outlines the therapeutic potential and challenges of precision disease interventions targeting Trm cells.

Various extracts from centipedes have therapeutic effects on liver cancer. This study aims to illustrate the impact and mechanism of centipede polypeptide (CP) on liver cancer. The suitable CP concentration and liver cancer cells were screened through CCK‐8 analysis. The expression of proteins was analysed by Western blot. The level of cytokines and markers was measured by ELISA and biochemical kits. The apoptosis rate of cells was analysed by TUNEL staining and flow cytometry. Histopathological changes were observed by HE staining. The expression of Ki‐67 and caspase‐3 was assessed by IHC staining. The combination of CP and p53 was simulated by molecular docking. 200 μg/mL CP and HepG2 cells were applied in experiments. CP significantly upregulated p53, TNF‐associated apoptosis‐inducing ligand (TRAIL), TRADD and TRAF expression in HepG2 cells and tumour tissues (p < 0.05), suggesting p53‐dependent activation of the TRAIL pathway. CP raised the levels of IL‐6, IL‐1β, TNF‐α, MDA and ROS, and decreased those of IL‐10, TGF‐β1 and SOD in HepG2 cell supernatant and serum of nude mice (p < 0.05). CP promoted cell apoptosis and reduced the levels of ALT and AST to inhibit the progression of cancer. Molecular docking showed that CP could bind stably to p53 (p < 0.05). Silencing of p53 restrained the activation of the p53/TRAIL pathway and reduced the level of inflammatory reaction and ferroptosis, thus reversing the therapeutic effect of CP on liver cancer (p < 0.05). CP affected the inflammatory reaction and ferroptosis of liver cancer cells through the p53/TRAIL pathway.