Objective To investigate the effect of overexpression of miR-30b on the proliferation,cell cycle,apoptosis and invasion of gastric cancer cell line SGC-7901 and AGS,and the inhibitory effect on the tumor formation in vivo.Methods SGC-7901 and AGS cells were transfected with miR-30b mimics and miR-control,and qRT-PCR was used to detect the expression levels of miR-30b.Western blot assay was used to detect the expression of eIFSA2 protein.CCK-8 assay was used to measure the cell proliferation.Flow cytometry was used to analyze cell cycle and apoptosis.Transwell assay was used to detect cell invasion.In addition,the SGC-7901 and AGS cells transfected with miR-30b mimics and miR-control were injected into nude mice to observe the tumor formation and the expression of eIFSA2 protein in vivo.Results Results of qRT-PCR showed that the relative expression of miR-30b was significantly higher than that of miR-control group (P ＜ 0.05).Western blot assay showed that the expression of eIF5A2 protein was decreased in miR-30b mimics group.CCK-8 assay showed that cell proliferation was inhibited in miR-30b mimics group.The result of flow cytometry showed that the cell cycle decreased and the apoptosis increased in miR-30b group.Transwell assay showed that the cell invasion was significantly lower in miR-30b group than that of control group (P ＜ 0.05).Overexpression of miR-30b inhibited the formation of tumor and decreased the expression of eIF5A2 protein in vivo.Conclusion Overexpression of miR-30b inhibits the proliferation,invasion and tumor formation of gastric cancer cells,and reduces the expression of eIF5A2 protein,which provides a potential target for gastric cancer treatment.

Pien Tze Huang(PZH),a class-1 nationally protected traditional Chinese medicine(TCM),has been used to treat liver diseases such as hepatitis;however,the effect of PZH on the progression of sepsis is un-known.Here,we reported that PZH attenuated lipopolysaccharide(LPS)-induced sepsis in mice and reduced LPS-induced production of proinflammatory cytokines in macrophages by inhibiting the acti-vation of mitogen-activated protein kinase(MAPK)and nuclear factor-kappa B(NF-κB)signalling.Mechanistically,PZH stimulated signal transducer and activator of transcription 3(STAT3)phosphory-lation to induce the expression of A20,which could inhibit the activation of NF-κB and MAPK signalling.Knockdown of the bile acid(BA)receptor G protein-coupled bile acid receptor 1(TGR5)in macrophages abolished the effects of PZH on STAT3 phosphorylation and A20 induction,as well as the LPS-induced inflammatory response,suggesting that BAs in PZH may mediate its anti-inflammatory effects by acti-vating TGR5.Consistently,deprivation of BAs in PZH by cholestyramine resin reduced the effects of PZH on the expression of phosphorylated-STAT3 and A20,the activation of NF-κB and MAPK signalling,and the production of proinflammatory cytokines,whereas the addition of BAs to cholestyramine resin-treated PZH partially restored the inhibitory effects on the production of proinflammatory cytokines.Overall,our study identifies BAs as the effective components in PZH that activate TGR5-STAT3-A20 signalling to ameliorate LPS-induced sepsis.