Background
Increasing evidence suggests that microRNAs (miRNAs) play critical roles in cancer progression. Therefore, investigating the function of miRNAs that are aberrantly expressed in gastric cancer (GC) and characterizing the involved underlying mechanism are essential for the treatment of gastric cancer. MiR-138-5p was found to be down-regulated in multiple cancers, which acted as a tumor suppressor in cancer progression; however, whether and how miR-138-5p regulates the malignant behaviors of GC has not been fully understood.
Conclusion
Our results demonstrated the anti-cancer role of miR-138-5p in GC by targeting DEK, which suggested miR-138-5p as a potential therapeutic target for the treatment of patient with GC.
Methods
The level of miR-138-5p in GC tissues and cell lines was detected by RT-qPCR. The effects of miR-138-5p on the growth of GC cells were evaluated by the in vitro Cell Counting Kit-8 (CCK-8) assay, cell apoptosis, cell cycle analysis, wound-healing assay, and in vivo xenograft mice model. The targets of miR-138-5p were predicted using the miRDB online tool, confirmed by luciferase report assay and Western blot.
Results
MiR-138-5p was frequently decreased in GC tissues and cell lines. Decreased expression of miR-138-5p was significantly associated with the lymph node metastasis of GC patients. Overexpression of miR-138-5p suppressed GC cell proliferation, migration, increased cell apoptosis as well as inhibited the tumor growth in vivo. DEK oncogene was predicted as a potential target of miR-138-5p. MiR-138-5p bound the 3'-UTR of DEK and inhibited the level of DEK in GC cells. Restoration of DEK abrogated miR-138-5p overexpression-mediated suppression of GC cell proliferation and cell cycle arrest.