MiR-216b regulates the tumorigenesis of gastric cancer by targeting PXN.

Abstract Background Accumulating evidence has demonstrated that microRNAs (miRNAs) are associated with tumorigenesis. miR-216b can play a vital role in the genesis and development of gastric cancer (GC), and its molecular mechanisms require further elucidation. Methods The biological effects of miR-216b in GC cells were investigated by MTT, transwell assays, and cell cycle. Western blot and luciferase assay were performed to demonstrate the direct binding of miR-216b on PXN 3′UTR. Furthermore, MTT, colony formation assays, transwell assays, and flow cytometry analysis, as well as xenograft mice model, were used to measure the effects of miR-216b-PXN on GC cell proliferation, migration, and invasion indicated by in vitro and in vivo. Results Our results showed that miR-216b acted as a tumor suppressor in GC progression. miR-216b overexpression suppressed GC cell proliferation, migration, and invasion in vitro. Luciferase reporter assays identified paxillin (PXN) as a novel target gene of miR-216b. PXN overexpression could partially rescue miR-216b-induced the inhibitory effects in GC cells. Besides, overexpression of miR-216b contributed to the activation of PI3K/AKT signaling via partly regulating PXN in GC cells. Conclusions The above results showed that miR-216b could offer a novel therapeutic avenue by targeting PXN in GC.