Resveratrol inhibits the proliferation, invasion, and migration, and induces the apoptosis of human gastric cancer cells through the MALAT1/miR-383-5p/DDIT4 signaling pathway

Background: We aimed to study the effects and potential mechanism of resveratrol (RS) in gastric cancer Methods: The human GC cell line SGC7901 was treated with different concentrations of RS (0, 1, 5 ??M) for 24 hours. The messenger ribonucleic acid or protein expressions levels of metastasisassociated lung adenocarcinoma transcript 1 (MALAT1), micro ribonucleic acid???383-5p (miR-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), MALAT1-interfering RNA (si-MALAT1), si-DDIT4 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 MALAT1, 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 MALAT1 meanwhile, the above anti-cancer effects were more significant (all P<0.05). Target prediction and the luciferase-reporter gene analysis showed that MALAT1 targeted miR-383-5p (P<0.05). When suppressing the expression of MALAT1 and miR-383-5p, the anti-cancer effects caused by the silencing of MALAT1 were absent (all P<0.05). We also found that miR-383-5p targeted DDIT4 protein. When the expression of miR-383-5p and DDIT4 in the GC cells was inhibited, the promoting cancer effects caused by the inhibition of miR-383-5p 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 (MALAT1)/miR-383-5p/DDIT4 pathway and induced apoptosis.