Background Long noncoding RNAs (lncRNAs) are from the family of noncoding RNAs. Existing studies have shown that lncRNAs are involved in many biological processes and are strongly related to the occurrence and development of tumors. Recent studies have indicated that lncRNA GIHCG participates in the progression of many cancers by adjusting cell proliferation and migration. Gastric cancer (GC) is a prevalent malignant tumor that arises from gastric epithelium. This study mainly explored the influence of GIHCG on GC and its underlying mechanism. Methods GIHCG expression was detected in GC through quantitative real‐time polymerase chain reaction while the relationship of GIHCG with miR‐1281 and miR‐1281 with TLE1 was verified using dual luciferase reporter gene assay. The influence of GIHCG, miR‐1281 and TLE1 on cell function was verified using cell counting Kit‐8 (CCK‐8) and Transwell experiment. Results In GC, GIHCG was significantly overexpressed and significantly increased cell proliferation and migration, with the possible mechanism of upregulatingTLE1 expression through adsorption of miR‐1281. Conclusion Taken together, we revealed the role of GIHCG/miR‐1281/TLE1 in GC and provided a new perspective.
Background This study was designed to illustrate the effects and latent mechanism of lncRNA maternally expressed gene 3 (MEG3) on intracerebral hemorrhage (ICH)-induced brain injury. Material/Methods An ICH rat model was generated to determine the role of lncRNA MEG3 in ICH. The interaction between lncRNA MEG3 and microRNA (miR)-181b were confirmed by Starbase and dual-luciferase reporter assay. One hour (h) or 3 days after ICH stimulation, rat neurological injury was evaluated by modified Neurological Severity Score (mNSS). Brain water content and cell apoptosis were assessed using brain edema assessment and flow cytometry (FCM), respectively. Caspase3 activity was also determined. Enzyme-linked immunosorbent assay (ELISA) was applied to evaluate the levels of pro-inflammatory cytokines. Moreover, the representative biomarkers of oxidative stress were evidenced using detection kits. Results The lncRNA MEG3 level in ICH rat brain tissues was higher than that in the sham group. miR-181b was a direct target of lncRNA MEG3 and it was downregulated in brain tissues of ICH rats. Notably, we found that neurobehavioral scores, brain water content, and neuronal apoptosis were decreased and caspase3 activity was reduced in MEG3-shRNA-treated ICH rats, while we observed the opposite result in ICH+MEG3-shRNA+miR-181b inhibitor rats. Further analyses revealed that MEG3-shRNA inhibited inflammatory cytokines release and reduced oxidative stress. All these results were reversed by miR-181b inhibitor. In addition, MEG3-shRNA activated the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) pathway, which was reversed by miR-181b inhibitor. Conclusions MEG3-shRNA restrained oxidative stress and inflammation following ICH in an miR-181b-dependent manner.
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