Liu Y.,Jining No. 1 Peoples Hospital |
Wang Y.,Jining No. 2 Peoples Hospital |
Yang N.,Qingdao University |
Wu S.,Jining No. 1 Peoples Hospital |
And 2 more authors.
Molecular Medicine Reports | Year: 2015
Postmenopausal osteoporosis (PO) is a common disease in females >50 years of age worldwide and is becoming an increasing burden to society. The present study aimed to assess the molecular mechanism of PO using bioinformatic methods. The gene expression data from patients with PO and normal controls were downloaded from the ArrayExpress database provided by European Bioinformatics Institute. Following the screening of the differentially expressed genes (DEGs) using the Limma package in R language, Kyoto Encyclopedia of Genes and Genomes pathways enrichment analysis was performed using the Database for Annotation, Visualization and Integrated Discovery online tools. Sequentially, modulators of the DEGs, including transcription factors (TFs) and microRNAs, were predicted by the ChIP Enrichment Analysis databases and WEB-based GEne SeT AnaLysis Toolkit system, respectively. In addition, the protein-protein interaction network of DEGs was constructed via the search tool for the retrieval of interacting genes and then the functional modules were further analyzed via the clusterMaker package and The Biological Networks Gene Ontology package within the Cytoscape software. A total of 482 DEGs, including 279 upregulated and 203 downregulated DEGs, were screened out. DEGs were predominantly enriched in the pathways of fatty acid metabolism, cardiac muscle contraction and DNA replication. TFs, including SMAD4, in addition to microRNAs, including the microRNA-125 (miR-125) family, miR-331 and miR-24, may be the modulators of the DEGs in PO. In addition, the five largest modules were identified with TTN, L1G1, ACADM, UQCRC2 and TRIM63 as the hub proteins, and they were associated with the biological processes of muscle contraction, DNA replication initiation, lipid modification, generation of precursor metabolites and energy, and regulation of acetyl-CoA biosynthetic process, respectively. SMAD4, CACNG1 and TRIM63 are suggested to be important factors in the molecular mechanisms of PO, and miR-331 may be novel potential biomarker for PO. Source
Sun K.,Shandong Qianfoshan Hospital |
Guo M.,Jining Medical University |
Gao H.,Jining No. 2 Peoples Hospital |
Liu K.,Jining Medical University |
And 4 more authors.
Cancer Causes and Control | Year: 2015
Purpose: To investigate the association between fish consumption and n-3 polyunsaturated fatty acids (n-3 PUFA) and the risk of hepatocellular carcinoma (HCC). Methods: We identified eligible studies in MEDLINE and EMBASE up to July 2014 and the reference lists of original studies and review articles on this topic. Summary relative risks (SRR) with their 95 % confidence intervals (CI) were calculated with a random effects model. Results: Eleven studies (three cohort studies, seven retrospective case–control studies, and one nested case–control study) met eligibility criteria. Ten articles investigated fish consumption, two articles investigated n-3 PUFA, and two articles investigated alpha-linolenic acid (ALA). The current data suggest that fish consumption was associated with 35 % reduction in HCC risk (highest vs. lowest category SRRs = 0.65, 95 % CI 0.51–0.79; test for heterogeneity p = 0.057, I2 = 44.1 %). n-3 PUFA was associated with 51 % reduction in HCC risk (highest vs. lowest category SRRs = 0.49, 95 % CI 0.19–0.79). However, no significant inverse association was found in ALA (SRRs = 0.70, 95 % CI 0.30–1.10). Conclusion: Our meta-analysis of observational studies provides evidence that fish consumption and n-3 PUFA has inverse association with the risk of HCC. © 2014, Springer International Publishing Switzerland. Source
Xie P.,Tsinghua University |
Xie P.,Beijing Institute of Radiation Medicine |
Tang Y.,Beijing Institute of Radiation Medicine |
Shen S.,Beijing Institute of Radiation Medicine |
And 8 more authors.
Biochemical and Biophysical Research Communications | Year: 2011
Krüppel-like factor 2 (KLF2) has been demonstrated to be essential for normal lung development, erythroid differentiation, T-cell differentiation, migration and homing. However, the mechanisms underlying the regulation of KLF2, in particular its responsible E3 ligase is still unclear. Here we show that the homologous to E6AP carboxyl terminus (HECT)-type ubiquitin ligase Smad ubiquitination regulatory factor 1 (Smurf1) interacts with and targets KLF2 for poly-ubiquitination and proteasomal degradation specifically in lung cancer H1299 cells. The catalytic ligase activity of Smurf1 is required for it to regulate KLF2. Consequently, Smurf1 represses the transcriptional factor activity of KLF2 and regulates the expression its downstream genes such as CD62L and Wee1. This study provided the first evidence that Smurf1 functions as an E3 ligase to promote the ubiquitination and proteasomal degradation of KLF2. © 2011 Elsevier Inc. Source