The elevated levels of these miRNAs were significantly de-escalated in GC samples compared with GU and the fold decrease valued 2.2 fold for miR-204 and 1.8 folds for miR-182.
By building the epithelial-mesenchymal transition (EMT) model in vitro through the addition of transforming growth factor beta 1 (TGF-β1), expressions of miR-204 and snai1 in the EMT model together with their respective effects on EMT were evaluated. miR-204 was significantly downregulated in GC tissues and invasive GC cells (P < 0.05).
Our results also showed that Rab40b is a target gene of miR-204 and further demonstrated that Rab40b is negatively correlated with miR-204 in GC tissues.
These data demonstrate that miR-204 plays an important role in regulating metastasis of gastric cancer, which is involved in post-transcriptional repression of SIRT1.