DICER-AS1 functions as competing endogenous RNA that targets CSR1 by sponging microRNA-650 and suppresses gastric cancer progression.

OBJECTIVE

This study explored the functional interactions between the long non-coding RNA DICER-AS1 and the cellular stress response 1 () 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 .

RESULTS

DICER-AS1 and 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 expression. Importantly, ectopic DICER-AS1 and expression inhibited cell proliferation and migration and suppressed xenograft tumorgenicity .

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 . These findings indicate that targeting DICER-AS1 and miR-650 could be a novel treatment for gastric cancer.