OBJECTIVE: To investigate the role of miR-519 in regulating the cell activity of gastric cancer. 
 METHODS: The expression of miR-519 was measured by qPCR. The protein expression of HuR was detected by Western blot. MTT assay was used to detect the cell activity of gastric cancer cells.
 RESULTS: The protein level of HuR in the gastric cancer cells was higher than that in the control cells. Over-expression of HuR resulted in the increase in the cell activity of gastric cancer (P<0.001). Suppression of HuR decreased the cell activity of gastric cancer (P=0.001). The miR-519 level in the gastric cancer cells was lower than that in the control cells (P=0.001). Over-expression of miR-519 decreased the protein level of HuR and the activity of gastric cancer cells.
 CONCLUSION MiR-may inhibit the gastric cancer cell activity through suppression of HuR expression.
Cell Line, Tumor ; Cell Proliferation ; ELAV-Like Protein 1 ; genetics ; metabolism ; Gene Expression Regulation, Neoplastic ; Humans ; MicroRNAs ; genetics ; metabolism ; Stomach Neoplasms ; genetics ; metabolism

OBJECTIVE: To investigate whether circular RNA circRSF1 regulates radiation-induced inflammatory phenotype of hepatic stellate cells (HSCs) by binding to HuR protein and repressing its function. METHODS: Human HSC cell line LX2 with HuR overexpression or knockdown was exposed to 8 Gy X-ray irradiation, and the changes in the expression of inflammatory factors (IL-1β, IL-6 and TNF-α) were detected by qRT-PCR. The expressions of IκBα and phosphorylation of NF-κB were detected with Western blotting. The binding of circRSF1 to HuR was verified by RNA pull-down assay and RNA-binding protein immunoprecipitation (RIP). The expressions of inflammatory factors, IκBα and the phosphorylation of NF-κB were detected after modifying the interaction between circRSF1 and HuR. RESULTS: Knockdown of HuR significantly up- regulated the expressions of IL-1β, IL-6 and TNF-α, decreased IκBα expression and promoted NF-κB phosphorylation in irradiated LX2 cells, whereas overexpression of HuR produced the opposite changes (P < 0.05). Overexpression or knockdown of circRSF1 did not significantly affect the expression of HuR. RNA pull-down and RIP experiments confirmed the binding between circRSF1 and HuR. Overexpression of circRSF1 significantly reduced the binding of HuR to IκBα and down-regulated the expression of IκBα (P < 0.05). Overexpression of circRSF1 combined with HuR overexpression partially reversed the up-regulation of the inflammatory factors, down-regulated IκBα expression and increased phosphorylation of NFκB in LX2 cells, while the opposite effects were observed in cells with knockdown of both circRSF1 and HuR (P < 0.05). CONCLUSION circRSF1 reduces IκBα expression by binding to HuR to promote the activation of NF-κB pathway, thereby enhancing radiation- induced inflammatory phenotype of HSCs.
Humans ; Hepatic Stellate Cells/radiation effects* ; Interleukin-6 ; NF-kappa B ; NF-KappaB Inhibitor alpha ; Phenotype ; RNA ; RNA, Circular/metabolism* ; Tumor Necrosis Factor-alpha ; ELAV-Like Protein 1/metabolism*