Long non-coding RNAs involved in metastasis of gastric cancer

Gastric cancer(GC) is one of the most frequently diagnosed malignant diseases. The molecular mechanisms of metastasis remain unclear. Recently, studies have shown that long non-coding RNAs(lncRNAs) play critical roles in metastasis. Therefore, deeper understanding of this mechanism could provide potential diagnostic tools and therapeutic targets for metastatic GC. This review focuses on dysregulated lncRNAs in GC metastases. Due to the identification of multiple diverse mechanisms involved in GC metastasis, we classified them into seven categories, including lncRNAs related to epithelialmesenchymal transition, regulation of degradation of extracellular matrix, angiopoiesis, vasculogenic mimicry, and immunologic escape. As the TNM stage is pivotal for evaluating the severity and prognosis of GC patients, we summarize the lncRNAs relevant to lymphatic metastasis, distant metastasis and TNM classification. This review summarizes the lncRNAs related to metastasis, which may provide insight into the mechanisms, and provide potential markers for prognostic prediction and monitoring the relapse of GC.

Cardioprotective Potential of Cymbopogon citratus Essential Oil against Isoproterenol-induced Cardiomyocyte Hypertrophy:Possible Involvement of NLRP3 Inflammasome and Oxidative Phosphorylation Complex Subunits

Objective:Cymbopogon citratus(DC.)Stapf is a medicinal and edible herb that is widely used for the treatment of gastric,nervous and hypertensive disorders.In this study,we investigated the cardioprotective effects and mechanisms of the essential oil,the main active ingredient of Cymbopogon citratus,on isoproterenol(ISO)-induced cardiomyocyte hypertrophy.Methods:The compositions of Cymbopogon citratus essential oil(CCEO)were determined by gas chromatography-mass spectrometry.Cardiomyocytes were pretreated with 16.9µg/L CCEO for 1 h followed by 10µmol/L ISO for 24 h.Cardiac hypertrophy-related indicators and NLRP3 inflammasome expression were evaluated.Subsequently,transcriptome sequencing(RNA-seq)and target verification were used to further explore the underlying mechanism.Results:Our results showed that the CCEO mainly included citronellal(45.66%),geraniol(23.32%),and citronellol(10.37%).CCEO inhibited ISO-induced increases in cell surface area and protein content,as well as the upregulation of fetal gene expression.Moreover,CCEO inhibited ISO-induced NLRP3 inflammasome expression,as evidenced by decreased lactate dehydrogenase content and downregulated mRNA levels of NLRP3,ASC,CASP1,GSDMD,and IL-1β,as well as reduced protein levels of NLRP3,ASC,pro-caspase-1,caspase-1(p20),GSDMD-FL,GSDMD-N,and pro-IL-1β.The RNA-seq results showed that CCEO inhibited the increase in the mRNA levels of 26 oxidative phosphorylation complex subunits in ISO-treated cardiomyocytes.Our further experiments confirmed that CCEO suppressed ISO-induced upregulation of mt-Nd1,Sdhd,mt-Cytb,Uqcrq,and mt-Atp6 but had no obvious effects on mt-Col expression.Conclusion:CCEO inhibits ISO-induced cardiomyocyte hypertrophy through the suppression of NLRP3 inflammasome expression and the regulation of several oxidative phosphorylation complex subunits.

The predictive value of serum S1P and STIM1 levels after PCI for in-stent restenosis and their correlation with angiogenesis and inflammatory response

Objective:To study the predictive value of serum S1P and STIM1 levels after percutaneous coronary intervention (PCI) for in-stent restenosis and their correlation with angiogenesis and inflammatory response.Methods:130 patients who received PCI in our hospital between June 2013 and December 2016 were selected and divided into restenosis group and non-restenosis group according to the coronary angiography results 6-24 months after PCI. The serum levels of S1P, STIM1, angiogenesis molecules and inflammation molecules were detected 24 hours after PCI.Results:Serum S1P, NO, VEGF, Angptl2 and Angptl4 levels of restenosis group were significantly lower than those of non-restenosis group while STIM1, IFN-γ, IL-18, VCAM-1, P-selectin and L-selectin levels were significantly higher than those of non-restenosis group;serum NO, VEGF, Angptl2 and Angptl4 levels of restenosis group with lower STIM1 were significantly higher those of restenosis group with normal STIM1;serum IFN-γ, IL-18, VCAM-1, P-selectin and L-selectin levels of restenosis group with lower S1P were significantly higher than those of restenosis group with normal S1P.Conclusion:The decreased serum S1P and increased STIM1 after PCI have prediction value for in-stent restenosis and are closely related to the angiogenesis disorder and inflammation activation.

Correlation of serum miR-148b expression with myocardial injury and myocardial fibrosis in patients with myocardial infarction

Objective:To study the correlation of serum miR-148b expression with myocardial injury and myocardial fibrosis in patients with myocardial infarction.Methods:A total of 130 patients who were diagnosed with acute myocardial infarction and 100 healthy subjects who received physical examination in Hanzhong Central Hospital between March 2013 and October 2016 were selected and enrolled in AMI group and control group respectively. Serum was collected, fluorescent quantitative PCR kit was used to detect miR-148b expression, and enzyme-linked immunosorbent assay kit was used to detect the contents of myocardial injury markers and myocardial fibrosis markers.Results:Serum miR-148b expression as well as CK-MB, cTnT, H-FABP, PICP, PIIINP, CTX-I, TGF-β1 and GDF-15 levels in AMI group was significantly higher than those in control group;serum CK-MB, cTnT, H-FABP, PICP, PIIINP, CTX-I, TGF-β1 and GDF-15 levels in AMI patients with high miR-148b expression were significantly higher than those in AMI patients with low miR-148b expression.Conclusion: Highly expressed miR-148b in serum of patients with myocardial infarction can promote myocardial injury and myocardial fibrosis.