In vivo and in vitro effects of microRNA‐124 on human gastric cancer by targeting JAG1 through the Notch signaling pathway

In this study, we aim to determine the function of miR‐124 on gastric cancer (GC) cells and the underlying mechanism that involves jaddeg1 (JAG1) and the Notch signaling pathway. GC tissues and adjacent tissues from 100 patients suffering from GC were selected. GC SGC‐7901 and AGS cells were selected and grouped into control, mimic‐NC, miR‐124 mimic, inhibitor‐NC, miR‐124 inhibitor, and miR‐124 inhibitor + si‐JAG1 groups. RT‐qPCR and a Western blotting assay were conducted to detect the expression of miR‐124, JAG1, and Notch signaling pathway‐related proteins (NICD, HES1, and HES5). MTS, wound‐healing, transwell assay and flow cytometry were performed to detect cell proliferation, migration, invasion, cell cycle distribution, and apoptosis, respectively. Compared with adjacent tissues, a lower miR‐124 expression and higher JAG1 expression were found in GC tissues. JAG1 is a direct target gene of miR‐124. Compared with the control group, the expression of JAG1, NICD, HES1, and HES5, cell invasion, migration, and proliferation in the miR‐124 mimic group were decreased, while the apoptosis rate was increased and cells were arrested at the G0/G1 phase. Compared with the miR‐124 inhibitor group, the expression of JAG1, NICD, HES1, and HES5, cell invasion, migration, and proliferation in the miR‐124 inhibitor + si‐JAG1 group were decreased, while the apoptosis rate and cell ratio at the G0/G1 phase were increased. The demonstration that miR‐124 inhibits GC cell growth supports the concept that miR‐124 functions as a tumor suppressor by a mechanism that involves translational repression of the JAG1 and the inhibition of Notch signaling pathway. The demonstration that miR‐124 inhibits GC cell growth supports the concept that miR‐124 functions as a tumor suppressor by a mechanism that involves translational repression of the JAG1 and the inhibition of Notch signaling pathway.