Acute myocardial infarction (AMI) is characterized by cardiomyocyte death followed by myocardial fibrosis, eventually leading to heart failure. Long non-coding (lnc)RNA X-inactive specific transcript (XIST) serves a vital role in the regulation of fibrosis. The aim of the present study was to determine whether myocardial fibrosis may be regulated by XIST and to elucidate the underlying mechanism. The relative mRNA expression levels of the target genes were evaluated using reverse transcription-quantitative polymerase chain reaction. Cell viability and apoptosis were determined using a Cell Counting Kit-8 assay and flow cytometry, respectively. The apoptosis and fibrosis-related protein expression levels were detected using western blot analysis. Finally, the interaction between XIST and microRNA (miR)-155-5p was analyzed using a luciferase reporter assay. XIST-overexpression increased proliferation and the expression level of the fibrosis-related proteins in the human cardiac fibroblast cells (HCFs). XIST directly targeted miR-155-5p and downregulated its expression, while miR-155-5p downregulation abolished the effect of XIST-silencing on cell viability and the expression level of the fibrosis-related proteins in the HCFs. XIST promoted cell proliferation and the expression level of fibrosis-related proteins by sponging miR-155-5p. Therefore, XIST may represent a novel effective target for AMI treatment.
The current evidence is weak and fails to show superiority of one modality over the other. EM is currently used primarily in highly selected cases, but there are reports of a broader applicability in trauma. High-quality randomized studies or large-scale registry data are needed to further comment on the relative merits or disadvantages of EM in comparison to OS.
Increasing evidence has demonstrated that lncRNAs are critical regulators in diverse biological processes, but the function of lncRNA in metabolic regulation remains largely unexplored. In this study, we evaluated the association between lncRNA and metabolic pathways and identified metabolism-related lncRNAs. Gastric cancer can be mainly subdivided into 2 clusters based on these metabolism-related lncRNA regulators. Comparative analysis shows that these subtypes are found to be highly consistent with previously identified subtypes based on other omics data. Functional enrichment analysis shows that they are enriched in distinct biological processes. Mutation analysis shows that ABCA13 is a protective factor in subtype C1 but a risk factor in C2. Analysis of chemotherapeutic and immunotherapeutic sensitivity shows that these subtypes tend to display distinct sensitivity to the same chemical drugs. In conclusion, these findings demonstrated the significance of lncRNA in metabolic regulation. These metabolism-related lncRNA regulators can improve our understanding of the underlying mechanism of lncRNAs and advance the research of immunotherapies in the clinical management of gastric cancer.
BACKGROUND: Immunomodulatory genes play significant roles in the regulation of immunological properties of gastric cancer, but the effect of epigenetic regulation of these genes on the immune properties is unknown. METHOD: I analyzed the methylation-expression correlation among all immunomodulators and compared with the non-immunomodulators. The association between epigenetically regulated immunomodulators (ERI) and tumor microenvironment is evaluated. A key immunomodulator TIGIT is further selected to investigate the potential value in the regulation of immunologic properties. Furthermore, the prognostic value and the immunotherapeutic potential of TIGIT are also explored. RESULT: Four genes are identified as ERIs based on the negative correlation between expression and methylation. Association analysis shows that three ERIs participate in the regulation of the immune microenvironment of gastric cancer. Among these ERIs, TIGIT is identified as a key immunomodulator. TIGIT is found to be significantly associated with immune properties. The high TIGIT expression group tends to display an active immune landscape. TIGIT expression is also found to be associated with survival and immunotherapeutic sensitivity. High TIGIT expression group has a favorable prognosis and is more likely to respond to immunotherapy than the low expression group. CONCLUSION: TIGIT is an epigenetically regulated immunomodulator of gastric cancer which can modify the immune activity and affect immunotherapeutic sensitivity. These findings can promote the research of epigenetic therapies and improve the survival of cancer patients by sensitizing tumors to immune therapies.
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