Effects of silencing hsa_circ_0015326 on proliferation, migration, invasion, and apoptosis of epithelial ovarian cancer cells.

Although the treatment of ovarian cancer has made great progress, there are still many patients who are not timely detected and given targeted therapy due to unknown pathogenesis. Recent studies have found that hsa_circ_0015326 is upregulated in ovarian cancer and is involved in the proliferation, invasion, and migration of ovarian cancer cells. However, whether hsa_circ_0015326 can be used as a new target of ovarian cancer needs further investigation. Therefore, the effect of hsa_circ_0015326 on epithelial ovarian cancer was investigated in this study. At first, si-hsa_circ_0015326 lentivirus was transfected into epithelial ovarian cancer cells. Then real-time fluorescence quantitative PCR (qRT-PCR) was used to detect hsa_circ_0015326 level. The proliferation of ovarian cancer cells was detected by CCK-8 assay. The horizontal and vertical migration abilities of the cells were detected by wound-healing assay and Transwell assay, respectively. Transwell assay was also used to determine the invasion rate. As for the apoptosis rate, it was assessed by flow cytometry. As a result, the expression level of hsa_circ_0015326 in A2780 and SKOV3 was found to be higher than that in IOSE-80. However, after transfecting si-hsa_circ_0015326 and si-NC into the cells, the proliferation, migration, and invasion abilities of A2780 and SKOV3 cells in the si-hsa_circ_0015326 group were significantly reduced in comparison to those in the si-NC and mock groups, while their apoptosis rates were elevated. Collectively, silencing hsa_circ_0015326 bears the capability of inhibiting the proliferation, migration, and invasion of ovarian cancer cells while increasing apoptosis rate. It can be concluded that hsa_circ_0015326 promotes the malignant biological activities of epithelial ovarian cancer cells.

[Expression of NR1 mRNA of NMDA receptor by gastrodine on hypoxia injury in cultured rat cerebral cortical neurons].

OBJECTIVE: To investigate the effect of gastrodine on the expression of NR1 mRNA of NMDA receptor in cultured rat cerebral cortical neurons injury induced by hypoxia. METHOD: The injury models of cultured rat cerebral cortical neurons was made by hypoxia and hypoglucose. The concentration of 13, 26, 52 mg x L(-1) of gastrodine was respectively added to the injured cells. The R-PCR technique was used to study the expression of NR1 mRNA of NMDA receptor. RESULT: The expression of NR1 mRNA increased markedly in hypoxia and hypoglucose injured cells, the increased expression can be weakened by gastrodine, more significant effect was found in the concentration of 26 mg x L(-1) 52 mg x L(-1). CONCLUSION: Gastrodine may act as a neuro - protector by weakening the expression of NR1 mRNA in cultured rat cerebral cortical neurons injury induced by hypoxia and hypoglucose.