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.

Abstract

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