Anoikis is a newly discovered form of apoptosis that was originally identified in the extracellular matrix (ECM).Recent studies have reported that anoikis is central to cancer metastasis. Here, SNCG was identified as hub anoikis-associated gene in GC and associated with prognosis of patients with GC. To screen the hub anoikisassociated genes connected to GC, the database of Cancer Genome Atlas (TCGA) was employed. For further validating these identified genes, the Gene Expression Omnibus (GEO) dataset was applied, and Western blotting and quantitative Real-Time PCR were carried out. To identify hub genes, we conducted the analyses of univariate Cox regression, differential expression, and weighted gene co-expression network analysis (WGCNA). According to the identified hub genes, we constructed a model of prognosis. Following complex analysis, SNCG was finally identified as hub anoikis-associated gene in GC. Indeed, K-M and receiver operating characteristic analyses suggested that the expression patterns of SNCG can be used as prognostic factors for GC survival. The expression and survival trends of SNCG were verified in the validation cohort and in vitro experimental analyses. The analysis of immune cell infiltration showed that the infiltrated immune cells varied among patients with GC and gene SNCG. Furthermore, due to the significant association of the constructed risk signature with patient age and survival, this risk signature can be used to predict the prognosis of GC. We suggest that SNCG was served as hub anoikis-associated gene in GC. Meanwhile, SNCG may have prognostic potential for overall patient survival.
BACKGROUND: Propofol is an anesthetic agent and can impede the progression of human diseases. Circular RNA (circRNA) circ_0003645 has been identified to promote the development of atherosclerosis (AS). This study aimed at the functional mechanism of propofol and circ_0003645 in AS. METHODS: AS cell model was established by treatment of oxidized low-density lipoprotein (ox-LDL) in human umbilical vein endothelial cells (HUVECs). Cell viability or apoptosis detection was performed by Cell Counting Kit-8 (CCK-8) assay and flow cytometry. Circ_0003645, microRNA-149-3p (miR-149-3p) and tumor necrosis factor receptor-associated factor 7 (TRAF7) levels were determined by the quantitative real-time polymerase chain reaction (qRT-PCR). Inflammatory cytokines were examined using enzyme-linked immunosorbent assay (ELISA). Protein analysis was conducted by western blot. The interaction of miR-149-3p and circ_0003645 or TRAF7 was analyzed using dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay. RESULTS: Treatment of ox-LDL inhibited cell viability and enhanced apoptosis in HUVECs to establish the AS cell model. Propofol protected against cell viability inhibition and apoptosis promotion in AS cell model. Circ_0003645 expression was downregulated by propofol in AS cell model. Propofol alleviated cell apoptosis and inflammation by decreasing the circ_0003645 level. Circ_0003645 targeted miR-149-3p, and circ_0003645/miR-149-3p axis was involved in the functional regulation of propofol. TRAF7 was the target of miR-149-3p. Inhibition of miR-149-3p affected the function of propofol by upregulating the TRAF7 expression. Circ_0003645 sponged miR-149-3p to induce the upregulation of TRAF7 following propofol treatment. CONCLUSION: It has been suggested that propofol acted as an inhibitor against the ox-LDL-induced cell injury by the circ_0003645/miR-149-3p/TRAF7 axis.
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