ABSTRACT
Objective:To explore the expression of long non-coding RNA (lncRNA) CDK5RAP3 in gastric cancer tissue and its regulatory effect on gastric cancer cell proliferation and invasion.Methods:The expression differences of CDK5RAP3 in gastric cancer tissues and adjacent tissues were analyzed by TCGA database. By transfecting the pcDNA3.1-CDK5RAP3 plasmid into Hs-746T cells, a gastric cancer cell line overexpressing CDK5RAP3 (CDK5RAP3 group) was constructed, and the pcDNA3.1 plasmid was transfected into Hs-746T cells as a control group. The changes of CDK5RAP3 expression in the two groups of cells were detected by real-time quantitative PCR (qRT-PCR). The effects of overexpression of CDK5RAP3 on the proliferation and invasion of Hs-746T cells were detected by CCK-8 assay and Transwell assay, respectively. The binding sites of CDK5RAP3 and miR-223-3p were predicted by the starBase v2.0 database. The direct binding of CDK5RAP3 and miR-223-3p was verified by dual-luciferase reporter gene experiment. The expression levels of miR-223-3p in Hs-746T cells in each group were detected by qRT-PCR. Western blot was used to detect the expression levels of proliferation proteins and invasion proteins in Hs-746T cells in each group. The experimental data were analyzed by SPSS 17.0 software, and the measurement data conforming to the normal distribution were expressed as Mean±SD. The t-test was used to compare between two groups, and the one-way analysis of variance was used to compare the means of multiple groups. Results:Compared with adjacent tissues, the expression level of CDK5RAP3 in gastric cancer tissues was significantly lower ( P<0.01). The expressions of CDK5RAP3 in Hs-746T cells in the control group and CDK5RAP3 group were (1.08±0.77) and (10.63±2.14), respectively, and the difference was statistically significant ( P<0.01). Up-regulation of CDK5RAP3 significantly decreased the proliferation activity of Hs-746T cells ( P<0.05). The number of invasive cells in the control group and CDK5RAP3 group were (137.80±28.72) and (57.76±24.95), respectively, and the difference was statistically significant ( P<0.01). CDK5RAP3 could directly bind miR-223-3p ( P<0.01). The expression of miR-223-3p in Hs-746T cells in control group and CDK5RAP3 group were (6.22±1.20) and (1.01±0.98), respectively, and the difference was statistically significant ( P<0.01). Compared with the control group, up-regulation of CDK5RAP3 significantly reduced the expression levels of proliferation and invasive proteins. Conclusion:The expression of CDK5RAP3 is low in gastric cancer tissue, and CDK5RAP3 inhibits the proliferation and invasion of gastric cancer Hs-746T cells by targeting miR-223-3p.
ABSTRACT
Objective To observe the protective effect of Racecadotril combined with Succinate Injection on myocardial injury in children with rotavirus enteritis and explore its clinical significance.Methods Totally 116 cases of children with rotavirus enteritis from Huangshi Traditional Chinese Medicine ofEdong Healthcare Group were selected in this study.Patients were randomly divided into Racecadotril control group (n =58) and Racecadotril combined with Succinate Injection observation group (n =58).The levels of CK,CK-MB,LDH,IL-17,IL-6,and TNF-α were detected by ELISA analysis.The rates of clinic effects and adverse reaction were compared.Results There was no significant difference of CK,CK-MB,LDH,IL-17,IL-6,and TNF-α between two groups before treatment.After treatment,they were all decreased in two groups (P ＜ 0.05,0.01).However,they were all lower in observation group than those in control group after treatment (P＜0.05).The rate of clinic effects was 94.8％ in observation group,which was higher than 81.0％ in control group (P ＜ 0.05).The rate of adverse reaction was 8.6％ in observation group and 6.9％ in control group.There was no significant difference between two groups.Conclusion Racecadotril combined with Succinate Injection inhibits the inflammatory response to protect myocardial injury in RVE children,with significantly clinical efficacy and safety.