Resveratrol inhibits the proliferation, invasion, and migration, and induces the apoptosis of human gastric cancer cells through the signaling pathway.

BACKGROUND

We aimed to study the effects and potential mechanism of resveratrol (RS) in gastric cancer (GC).

METHODS

The human GC cell line SGC7901 was treated with different concentrations of RS (0, 1, 5 µM) for 24 hours. The messenger ribonucleic acid or protein expressions levels of metastasis-associated lung adenocarcinoma transcript 1 (), micro ribonucleic acid-383-5p (), and DNA damage-inducible transcript 4 (DDIT4) in GC cells were determined by Western blot and quantitative real-time polymerase chain assays. Cells were then transfected with miR-383-5p inhibitor (inhibitor), inhibitor negative control (NC), -interfering RNA (si-), si- and negative interference control (si-NC). The Cell Counting Kit-8 method, scratch assay, and transwell assay were performed to evaluate cell proliferation, migration, and invasion. Additionally, flow cytometry was used to examine apoptosis, and the target relationship was examined by a luciferase-reporter gene analysis.

RESULTS

RS treatment downregulated the expression of , repressed cell proliferation, inhibited cell migration and invasion (all P<0.05), and induced apoptosis (P<0.05) in GC cells. When the cells were treated with RS and inhibited the expression of meanwhile, the above anti-cancer effects were more significant (all P<0.05). Target prediction and the luciferase-reporter gene analysis showed that targeted (P<0.05). When suppressing the expression of and , the anti-cancer effects caused by the silencing of were absent (all P<0.05). We also found that miR-383-5p targeted protein. When the expression of and in the GC cells was inhibited, the promoting cancer effects caused by the inhibition of were reversed (all P<0.05).

CONCLUSIONS

This study found that RS inhibited the proliferation, migration, and invasion of human GC cells through the metastasis-associated lung adenocarcinoma transcript 1 ()/ pathway and induced apoptosis.