Background Gastric cancer (GCa) is one of the six major malignancies in the world with low survival rate. Although there are advances in therapeutic approaches, the prognosis of patients with GCa remains not optimistic. Therefore, this study aimed to evaluate the prognostic value of miR-324-5p, as well as its functional role in GCa progression. Methods The expression of miR-324-5p in tumor tissues and cell lines was examined using real-time quantitative PCR. The prognostic value of miR-324-5p in patients with GCa was evaluated by Kaplan-Meier survival curve and Cox regression analysis. Gain- and loss-of-function experiments were performed to evaluate the biological function of miR-324-5p during the progression of GCa, and a target gene of miR-324-5p was proposed. Results The expression of miR-324-5p was up-regulated in GCa tissues and cell lines. Patients with high expression of miR-324-5p had more cases with positive lymph node metastasis, advanced TNM stage, and worse overall survival compared with patients with low expression. The elevated miR-324-5p was an independent prognostic indicator of GCa. In addition, the inhibition of miR-324-5p could suppress GCa cell proliferation, migration and invasion and promote cell apoptosis, and PTEN was demonstrated to serve as a direct target of miR-324-5p in GCa progression. Conclusion The present study indicates that miR-324-5p overexpression predicts poor prognosis in GCa patients, and the reduction of miR-324-5p can inhibit GCa biological processes. PTEN is a target gene of GCa, which may mediate the biological function of miR-324-5p in GCa progression.
Objective This study explored the functional interactions between the long non-coding RNA DICER-AS1 and the cellular stress response 1 ( CSR1) gene in gastric cancer. Methods Quantitative polymerase chain reaction (qPCR) and western blotting were used to measure DICER-AS1, CSR1, and miR-650 expression levels. Gastric cancer cell line proliferation and migration abilities were analyzed using the MTT and transwell migration and invasion assays, respectively. Bioinformatic analysis and dual luciferase reporter assays were employed to study the functional interactions among miR-650, DICER-AS1, and CSR1. Results DICER-AS1 and CSR1 expression levels were significantly decreased in gastric cancer tissues compared with normal tissues, and qPCR analysis showed that miR-650 was upregulated in gastric cancer tissues. Bioinformatic analysis and dual luciferase reporter assays revealed that DICER-AS1 functioned as a competing endogenous RNA that sponged miR-650, which in turn regulated CSR1 expression. Importantly, ectopic DICER-AS1 and CSR1 expression inhibited cell proliferation and migration in vitro and suppressed xenograft tumorgenicity in vivo. Conclusions These results suggest that DICER-AS1 functions as a competing endogenous RNA that regulates miR-650 to suppress proliferation and migration of gastric cancer cells by targeting CSR1. These findings indicate that targeting DICER-AS1 and miR-650 could be a novel treatment for gastric cancer.
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