BackgroundThe objective of this study was to investigate the role and mechanism of long non-coding RNA MIAT in gastric cancer (GC).MethodsReal-time PCR was used to determine MIAT level in 120 GC tissues, and in two gastric cancer cell lines. The clinicopathological characteristics of MIAT in GC patients were analyzed. Small interfering RNA specific for MIAT (si-MIAT) and lentivector for si-MIAT was performed to down-regulate MIAT expression in GC cells and in animal tumor model, respectively. The interaction of MIAT and miR-141 was measured by RNA pull-down assay and RNA immunoprecipitation. The biological function of si-MIAT on GC cell growth and metastasis were explored through flow cytometry assay, invasion and migration assay in vitro.ResultsMIAT was highly expressed in GC tissues and cell lines and correlated with differentiation degree, TNM stage, distant metastasis, and lymph node metastasis. MIAT knockdown inhibited GC growth and metastasis both in vitro and in vivo. Furthermore, MIAT acted as miR-141 sponge and regulated its target gene DDX5 expression. In BGC-823 and MGC-803 cells with si-MIAT, DDX5 overexpression resulted in an increase of cell proliferation, migration and invasion.ConclusionsOur data indicated that MIAT played an oncogenic role in GC growth and metastasis, and could serve as a novel molecular target for treating GC.Electronic supplementary materialThe online version of this article (10.1186/s13046-018-0725-3) contains supplementary material, which is available to authorized users.

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Objective: Celastrol, a plant triterpene, has anticancer effects by increase of apoptosis. In the present study, the mechanism of celastrol on gastric cancer cell apoptosis was examined. Methods: The effect of celastrol on PI3K/Akt and the NF-κB signaling pathway was evaluated with Western blot and luciferase reporter assay. miR-21 expression was determined using real-time PCR. miR-21 inhibitor and miR-21 mimic were used to downregulate and upregulate miR-21 expression, respectively. Results: It was identified that celastrol was capable of inducing apoptosis of gastric cancer cells, which was mediated via inhibiting the activation of PI3K/Akt and NF-κB. A strong activator of Akt, IGF-1 restored NF-κB activity in cells treated with celastrol. Celastrol could also significantly suppress miR-21 expression. Furthermore, miR-21 inhibitor could decrease phospho-Akt expression and NF-κB activity. Notably, upregulation of miR-21 expression can increase PI3K/Akt and NF-κB activity and decrease apoptosis of gastric cancer cells treated with celastrol, which could be reversed by PI3K inhibitor. Conclusions: Our data revealed that the effect of celastrol on apoptosis was due to miR-21 inhibiting the PI3K/Akt-dependent NF-κB pathway.