Conclusions
These results suggested that miR-411 functions as a tumor suppressor in GC through targeting SETD6/NF-κB pathway. Targeting miR-411 may be a novel clue for GC treatment.
Methods
We determined the expression level of miR-411 in GC cell lines. After synthetic miRNAs or SET domain containing 6 (SETD6) expression vectors transfection, cell proliferation, colony formation, and migration were examined. Moreover, the target of miR-411 was identified by luciferase activity reporter assay and Western blot assay.
Objective
MicroRNAs (miRNAs) affect almost all cell behaviors of human cancers including gastric cancer (GC). However, the biological role of miR-411 in GC remains to be elucidated. Materials and
Results
Results revealed that the miR-411 expression was significantly down-regulated in GC cell lines compared with normal colonic epithelial cells. Overexpression of miR-411 inhibits GC cell proliferation, colony formation, and migration, whereas the overexpression of SETD6 promotes cell proliferation, colony formation, and migration. Moreover, SETD6 was identified as a putative target of miR-411. In addition, we showed miR-411 regulates GC cell behaviors by targeting SETD6. The overexpression of SETD6 promoted the activation of the nuclear factor (NF)-κB signaling pathway. Conclusions: These results suggested that miR-411 functions as a tumor suppressor in GC through targeting SETD6/NF-κB pathway. Targeting miR-411 may be a novel clue for GC treatment.