Search

Objective To investigate the potential effects of long non-coding RNA (lncRNA) MINCR on lipopolysaccharide (LPS)-induced human alveolar epithelial cell line A549 damage and inflammation through targeted regulation of miR-223. Methods A549 cells were randomly divided into control group, LPS group, LPS+transfection group(Si NC group, Si MINCR group, miR-223 NC group, miR-223 mimic group, Si NC+miR-223 NC group, Si NC+miR-223 antagomir group, Si MINCR+miR-223 NC group, and Si MINCR+miR-223 antagomir group). RT-qPCR was performed to determine the expression levels of MINCR and miR-223; Flow cytometry was performed to determine the rate of apoptosis; ELISA was performed to determine the levels of serum tumor necrosis factor-α(TNF-α) and interleukin-6 (IL-6); Bioinformatics prediction and dual luciferase reporter gene assay were performed to verify the targeting relationship of MINCR and miR-223; Western blot was performed to test the expression levels of activated caspase-3 (cleaved caspase-3) and B-cell lymphoma-2(Bcl-2) proteins in the cells. Results There was a targeting relationship between MINCR and miR-223. Compared with the control group, the apoptosis rate, the level of TNF-α and IL-6, and the expression of MINCR, cleaved caspase-3 proteins in the LPS group were significantly increased (PPPPPPPConclusions Silencing the expression of lncRNA MINCR may target the activation of miR-223 expression, inhibit cell apoptosis and inflammation, and reduce LPS-induced damage of alveolar epithelial cells.

With the rapid development of the Internet, each platform often uses metadata to organize and manage system data resources. The system within the platform is closed so that metadata resources are dispersed and stored repeatedly, which increases the difficulty of metadata sharing and reduces the utilization of metadata. In order to solve this problem, this paper proposes a public metadata configuration management platform, which provides unified configuration and management of public metadata, provides configuration and shared metadata services by using Web Service technology, and improves data sharing efficiency by using Redis memory database. At present, a configuration management platform based on meteorological public metadata has been used in the meteorological big data platform, which not only improves the utilization of the platform common metadata, saves storage, but also improves the response speed of the service. This article abstracts the main functions of the configuration management platform, making the system design applicable to other similar metadata-based data sharing platforms.

Background: T‐cell immunoglobulin and immunoreceptor tyrosine‐based inhibitory motif domain (TIGIT) is an immune checkpoint molecule that suppresses CD8+ T‐cell function in cancer. However, the expression profile and functional significance of TIGIT in the immune microenvironment of lung adenocarcinoma (LUAD) remain elusive. Interleukin (IL)‐15 has emerged as a promising candidate for enhancing CD8+ T‐cell mediated tumour eradication. Exploring therapeutic strategies that combine IL‐15 with TIGIT blockade in LUAD is warranted. Methods: We investigated the regulatory network involving coinhibitory TIGIT and CD96, as well as costimulatory CD226 in LUAD using clinical samples. The potential role of TIGIT in regulating the pathogenesis of LUAD was addressed through a murine model with transplanted tumours constructed in Tigit−/− mice. The therapeutic strategy that combines TIGIT blockade with IL‐15 stimulation was verified using a transplanted tumour murine model and a patient‐derived organoid (PDO) model. Results: The frequency of TIGIT+CD8+ T cells was significantly increased in LUAD. Increased TIGIT expression indicated poorer prognosis in LUAD patients. Furthermore, the effector function of TIGIT+CD8+ tumour‐infiltrating lymphocytes (TILs) was impaired in LUAD patients and TIGIT inhibited antitumour immune response of CD8+ TILs in tumour‐bearing mice. Mechanistically, IL‐15 enhanced the effector function of CD8+ TILs but stimulated the expression of TIGIT on CD8+ TILs concomitantly. The application of IL‐15 combined with TIGIT blockade showed additive effects in enhancing the cytotoxicity of CD8+ TILs and thus further increased the antitumour immune response in LUAD. Conclusions: Our findings identified TIGIT as a promising therapeutic target for LUAD. LUAD could benefit more from the combined therapy of IL‐15 stimulation and TIGIT blockade. [ABSTRACT FROM AUTHOR]