Knockdown of long non-coding RNA PEG10 inhibits growth, migration and invasion of gastric carcinoma cells by up-regulating miR-3200

摘要

Gastric cancer is the major cause of cancer-related death worldwide. The aberrant expression of the PEG10 paternally expressed gene 10 is involved in the development of a range of cancers. Although the biological function and the underling mechanism of PEG10 in human gastric carcinoma are still unknown, LncRNA PEG10 knockdown could present a promising therapeutic strategy for the treatment of gastric cancer. Herein, the expression of PEG10, miR-3200 and AEG1 in human gastric carcinoma NCI-N87 cells was altered by cell transfection assay, and the cell viability, migration, invasion, and apoptosis were determined by trypan blue exclusion, Transwell assay and flow cytometry, respectively. Gene RNA and protein expression levels were analyzed by real-time PCR and Western blot and the Luciferase reporter assay determined miR-3200's target gene. JNK and Wnt signal pathway protein expressions were then tested by Western blot. While PEG10 up-regulation was evident in clinical samples its knockdown effectively inhibited gastric carcinoma cell viability, migration and invasion but promoted cell apoptosis. This tumor-suppressive effect by PEG10 knockdown can be provided by up-regulating miR-3200 in vitro and in vivo. AEG1 is a direct miR-3200 target gene and miR-3200 suppresses NCI-N87 cells by negative AEG1 regulation. Furthermore, miR-3200 up-regulation most likely blocks the JNK and Wnt pathways by down-regulating AEG1. Finally, PEG10 knockdown has a carcinostatic role by up-regulating miR-3200, and the JNK and Wnt pathway block during this process further regulates AEG1 in gastric carcinoma cells.