Background: Bronchopulmonary dysplasia (BPD) is a complex disorder resulting from interactions between genes and the environment. The precise molecular etiology of BPD remains unclear. This study aimed to determine potential biomarkers and possible therapeutic targets of BPD through competitive endogenous RNA (ceRNA) network analysis and lay the foundation for future clinical research. Methods: First, we downloaded the mRNA, miRNA, and long non-coding RNA (lncRNA) expression profiles of patients with BPD from the Comprehensive Gene Expression Database. We identified differentially expressed genes (DEGs), followed by functional enrichment analysis, construction of a protein-protein interaction network, and construction of ceRNA network. Results: We obtained1286 DEGs, 77 differentially expressed miRNAs, and 104 differentially expressed lncRNAs. Functional enrichment analysis showed that DEGs were mainly involved in B-cell receptor signaling pathways, asthma, FcRI signaling pathways, cell apoptosis, the intestinal immune network that produces IgA, and Th17 cell differentiation signaling pathways. We constructed ceRNA network based on the predicted relationship between lncRNA-miRNA and mRNA-miRNA, including 6 lncRNAs, 11 miRNAs, and 56 mRNAs. Conclusion: Through ceRNA network analysis, we identified six new lncRNAs that are potential biomarkers and therapeutic targets of BPD, thus opening up a new horizon for the prevention and treatment of BPD.
Background: Inflammatory cytokines are related to the occurrence and development of hepatocellular carcinoma (HCC). Objectives: Interleukin 6 (IL-6) is associated with the occurrence and prognosis of HCC, while Dicer inhibits HCC; accordingly, we checked whether Dicer regulates HCC by modulating the IL-6 pathway. Methods: The HCC cells of SMMC-7721 transfected with Dicer overexpression (pCMV-Dicer) and control (pCMV-NC) lentivirus were divided into 3 groups: The SMMC-7721, pCMV-NC, and pCMV-Dicer groups. The assays of cell proliferation, migration, and invasion were performed using cell counting, wound scratch, and transwell chamber assay. The IL-6 level was measured by flow cytometry bead-based immunoassays. All statistical analyses were analyzed using SPSS version 21 by the student t test and 1-way analysis of variance (ANOVA). Results: Dicer inhibited the secretion of IL-6 from HCC cells, as well as the growth of HCC related to proliferation, migration, and invasion. IL-6 incubation with pCMV-NC cells increased proliferation (from 24 hours to 72 hours; P < 0.05), migration (P = 0.008), and invasion (P = 0.85). In addition, IL-6 could reverse the inhibitory effect of Dicer on HCC cells related to proliferation (P < 0.01) and migration (P = 0.006) when incubated with pCMV-Dicer cells, whereas an IL-6 blocker of tocilizumab could enhance the Dicer-induced inhibition related to proliferation (P < 0.05), migration (P = 0.007), and invasion (P = 0.001) when incubated with pCMV-Dicer cells. Furthermore, Dicer could increase the inhibition efficiency of apatinib on HCC treatment by their cooperation in IL-6 downregulation. Conclusions: Dicer could inhibit HCC by the IL-6 pathway, which would be a potential target for HCC treatment. The Dicer inducer might be an enhancer of apatinib for HCC treatment.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.