DataSheet1_Metabolomics unveils the exacerbating role of arachidonic acid metabolism in atherosclerosis.PDF

Atherosclerosis is a complex vascular disorder characterized by the deposition of lipids, inflammatory cascades, and plaque formation in arterial walls. A thorough understanding of its causes and progression is necessary to develop effective diagnostic and therapeutic strategies. Recent breakthroughs in metabolomics have provided valuable insights into the molecular mechanisms and genetic factors involved in atherosclerosis, leading to innovative approaches for preventing and treating the disease. In our study, we analyzed clinical serum samples from both atherosclerosis patients and animal models using laser desorption ionization mass spectrometry. By employing methods such as orthogonal partial least-squares discrimination analysis (OPLS-DA), heatmaps, and volcano plots, we can accurately classify atherosclerosis (AUC = 0.892) and identify key molecules associated with the disease. Specifically, we observed elevated levels of arachidonic acid and its metabolite, leukotriene B4, in atherosclerosis. By inhibiting arachidonic acid and monitoring its downstream metabolites, we discovered the crucial role of this metabolic pathway in regulating atherosclerosis. Metabolomic research provides detailed insights into the metabolic networks involved in atherosclerosis development and reveals the close connection between abnormal metabolism and the disease. These studies offer new possibilities for precise diagnosis, treatment, and monitoring of disease progression, as well as evaluating the effectiveness of therapeutic interventions.</p

Additional file 2: Figure S2. of MicroRNA-1908 functions as a glioblastoma oncogene by suppressing PTEN tumor suppressor pathway

miR-1908 promotes migration and invasion in SNB19 cells. (A) Scratch assay shows the effect of miR-1908 on migration in SNB19 cells. (B) Matrigel assay shows the effect of miR-1908 on invasion in SNB19 cells. **P < 0.01 based on the Student t test. Error bars, SD. (JPEG 2042 kb

Additional file 1: Figure S1. of Overexpression of CTNND1 in hepatocellular carcinoma promotes carcinous characters through activation of Wnt/β-catenin signaling

The expression of CTNND1 was analysised with TCGA data. (JPG 115 kb

Additional file 6 of Transcriptome sequencing and metabolome analysis reveal the metabolic reprogramming of partial hepatectomy and extended hepatectomy

Additional file 6: Figure S3. Metabolomic cluster dendrogram of different samples

Additional file 10 of Transcriptome sequencing and metabolome analysis reveal the metabolic reprogramming of partial hepatectomy and extended hepatectomy

Additional file 10: Figure S7. The experimental workflow chart of this study

Additional file 1 of Transcriptome sequencing and metabolome analysis reveal the metabolic reprogramming of partial hepatectomy and extended hepatectomy

Additional file 1: Table S1. All the reserved genes for differential analysis, the genes in all groups with a mean expression of < 3 read counts were filtered out

Additional file 3 of Transcriptome sequencing and metabolome analysis reveal the metabolic reprogramming of partial hepatectomy and extended hepatectomy

Additional file 3: Table S2. Expression patterns of all 14,505 reserved genes in eHx vs. pHx

Silencing of DLGAP5 by siRNA Significantly Inhibits the Proliferation and Invasion of Hepatocellular Carcinoma Cells

<div><p>Background</p><p>The dysregulation of oncogenes and tumor suppressor genes plays an important role in many cancers, including hepatocellular carcinoma (HCC), which is one of the most common cancers in the world. In a previous microarray experiment, we found that DLGAP5 is overexpressed in HCCs. However, whether the up-regulation of DLGAP5 contributes to hepatocarcinogenesis remains unclear. </p> <p>Methodology/Principal Findings</p><p>In this study, we showed that DLGAP5 was significantly up-regulated in 76.4% (168 of 220) of the analyzed HCC specimens when compared with adjacent liver tissue. DLGAP5 overexpression was evident in 25% (22 of 88) of the HCC specimens without AFP expression, suggesting that DLGAP5 may be a novel biomarker for HCC pathogenesis. The silencing of DLGAP5 gene expression by RNA interference significantly suppressed cell growth, migration and colony formation in vitro. The expression level of DLGAP5 was also found to be related to the methylation level of its promoter in the HCC specimens. </p> <p>Conclusions/Significance</p><p>Taken together, these data suggest that the expression of DLGAP5 is regulated by methylation and that the up-regulation of DLGAP5 contributes to HCC tumorigenesis by promoting cell proliferation.</p> </div

Additional file 4 of Transcriptome sequencing and metabolome analysis reveal the metabolic reprogramming of partial hepatectomy and extended hepatectomy

Additional file 4: Figure S2. The expression pattern of TOP10 DEGs of 5 clusters of pHx and eHx

Additional file 5 of Transcriptome sequencing and metabolome analysis reveal the metabolic reprogramming of partial hepatectomy and extended hepatectomy

Additional file 5: Table S3. 1383 metabolites were filtered (variable coefficient ≥ 0.3) in all groups