Analysis of ceRNA network reveal potential lncRNA Biomarkers in macrophages resistant to vpr induced apoptosis
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PROVIDER: PRJNA869712 | ENA |
REPOSITORIES: ENA
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Project description:Backgrounds:Macrophages are one of HIV reservoirs. Vpr is essential for infection of macrophages by HIV-1 and has the potential to promote survival of macrophages, which could be a highly significant factor in the development and/or maintenance of macrophage viral reservoirs. However, the impact of vpr on macrophages resistance to apoptosis is yet to be comprehended. Methods:We determined the expression profiles of lncRNAs in THP1-MAC and THP1-MAC treated with Vpr peptides using microarray analysis. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed to explore their function. We also constructed competing endogenous RNA (ceRNA) networks with bioinformatics methods. Results：We identified 410 lncRNAs that were differentially expressed between THP1-MAC and THP1-MAC after Vpr peptides treatment. Significantly enriched GO terms and pathways were identified, some of which were linked to apoptosis and inflammatory responses. CeRNA analysis showed that lncRNA LINC02249 was paired with the most differentially expressed gene. qRT-PCR results confirmed the reliability of the microarray data. Conclusions：LINC02249 associated ceRNA network may play a role in macrophages resistant to vpr induced apoptosis. This will provide a new avenue for investigating the pathogenesis of macrophages resistant to vpr-induced apoptosis.
2022-08-16 | GSE211274 | GEO
Project description:Construction of ceRNA network based on an RNA‑seq shows prognostic lncRNA biomarkers in Perthes’ disease
2023-05-15 | GSE217908 | GEO
Project description:Cross-talk between competing endogenous RNAs (ceRNAs) play key roles in tumor development. In this study, we performed exon-level expression profiling on 26 glioblastomas (GBMs) and 6 controls to identify long non-coding RNAs (lncRNAs) of GBM initiation and progression using lncRNA-mediated ceRNA network (LMCN). The mRNA and lncRNA expression data, as well as miRNA-target interactions were firstly collected. Then, we used hypergeometric test to detect the lncRNA-mRNA interactions, followed by the construction of LMCN based on Pearson correlation coefficient. With the goal of investigation of the network organization, degree distribution of LMCN was performed. Next, the synergistic, competing lncRNA modules were identified using jActiveModule plug-in of Cytoscape. Moreover, we implemented the pathway analysis for its mRNAs in the module to explore the functions of significant lncRNAs. Using the criteria of degrees >50, 8 hub genes were identified, including EPB41L4A-AS1, ZRANB2-AS2, XIST, HOTAIR, TRAF3IP2-AS1, TPT1-AS1, PVT1 and DLG1-AS1. Furthermore, 1 synergistic, competitive module was identified. In this module, lncRNAs XIST and PVT1 were also the hubs in the synergistic, competing lncRNA module. Functional annotation demonstrated that 5 pathways were identified, including cytokine-cytokine receptor interaction, neuroactive ligand-receptor interaction, and mTOR signaling pathway. We have successfully identified several hubs (such as XIST and PVT1) and significant pathways (for instance, cytokine-cytokine receptor interaction, and neuroactive ligand-receptor interactions) for GBM via establishing the LMCN. These findings might offer potential biomarkers to early diagnose, and predict GBM prognosis in the future.
| S-EPMC6444437 | biostudies-literature
Project description:Lung adenocarcinoma (LUAD) is one of the most fatal malignant tumors harmful to human health. The complexity and behavior characteristics of long-non-coding RNA (lncRNA)-associated competing endogenous RNA (ceRNA) network in LUAD patients are still unclear. The purpose of this study was to elucidate the regulatory networks of dysregulated RNAs, view, and identify potential prognosis signatures involved in LUAD. The expression profiles of mRNAs, lncRNAs, and miRNAs were obtained from the TCGA database. In total, 2078 DEmRNAs, 257 DElncRNAs, and 101 DEmiRNAs were sorted out. A PPI network including 45 DEmRNAs was constructed. Ten hub genes in the PPI network associated with cell cycle-related pathways were identified and they played key roles in regulating cell proliferation. A total of three DEmiRNAs, seven DElncRNAs, and six DEmRNAs were enrolled in the ceRNA network. Except for certain genes without any published study reports, all the genes in the ceRNA network played an essential role in controlling tumor cell proliferation and were associated with prognosis in LUAD. Finally, based on step regression and Cox regression survival analysis, we identified four candidate biomarkers, including miR490, miR1293, LINC01740, and IGF2BP1, and established a risk model based on the four genes. Our study provided a global view and systematic dissection of the lncRNA-associated ceRNA network, and the identified four genes might be novel important prognostic factors involved in LUAD pathogenesis.
| S-EPMC7212445 | biostudies-literature
Project description:Three 293 cell-derivative cell line were constructed using commercially available Invitrogen Flp-In TREx 293 cells. The cell lines express wild type HIV-1 Vpr and two mutant Vprs, F72A/R73A and R80A. The mutant Vprs are defective in the Vpr cell cycle arrest phenotype. The cell lines were characterized for their ability to express Vpr at the RNA and protein levels and functionally for the ability of the inducibly expressed Vprs to arrest cell cycle progression at G2/M. To study whether certain host cell genes showed alterations in expression following induced expression of Vpr, we conducted a large scale host cell gene expression profiling study using microarray technologies. To determine whether the differential expression of certain genes was associated with Vpr-induced cell cycle arrest, we compared the gene expression pattern of wild type Vpr expressing cells with the pattern of Vpr mutant F72A/R73A- or R80A-Vpr expressing cells. Doxycycline-induced and uninduced and Flp-In TREx 293/Vpr cells were collected 0, 1, 2, 4, 6, 8, 12, 16 and 24 hours post induction (hpi). Doxycyclineinduced and uninduced Flp-In TREx 293/Blank cells were also collected as a reference for following experiments. Total RNA was isolated using RNAeasy Midi Kit (QIAGEN), according to the manufacturer's protocol. Human long oligonucleotide microarrays were obtained from the National Cancer Institute Microarray Facility, Advanced Technology Center (Gaithersburg, MD). The microarrays (Hs Operon V2) contained 22,434 oligonucleotide (60-70 mer) spots on a glass slide. 25 µg of total RNAs isolated from doxycycline-induced Flp-In TREx 293 stably transfected blank- and FLAG tagged-Vpr cells were reverse transcribed using an oligo (dT) primer and aminoallyl-dNTP (Amersham Pharmacia). Unincorporated dNTPs were removed with QIAquick PCR purification kit (QIAGEN). Purified cDNA was processed for coupling reaction with Cy 5 or Cy 3-ester dye, respectively. Keywords: other
2006-02-10 | GSE2296 | GEO
Project description:Background:Hepatocellular carcinoma (HCC) is the most common primary liver cancer in the world, with a high degree of malignancy and recurrence. The influence of the ceRNA network in tumor on the biological function of liver cancer is very important, It has been reported that many lncRNA play a key role in liver cancer development. In our study, integrated data analysis revealed potential eight novel lncRNA biomarkers in hepatocellular carcinoma. Methods:Transcriptome data and clinical data were downloaded from the The Cancer Genome Atlas (TCGA) data portal. Weighted gene co-expression network analysis was performed to identify the expression pattern of genes in liver cancer. Then, the ceRNA network was constructed using transcriptome data. Results:The integrated analysis of miRNA and RNAseq in the database show eight novel lncRNAs that may be involved in important biological pathways, including TNM and disease development in liver cancer. We performed function enrichment analysis of mRNAs affected by these lncRNAs. Conclusions:By identifying the ceRNA network and the lncRNAs that affect liver cancer, we showed that eight novel lncRNAs play an important role in the development and progress of liver cancer.
| S-EPMC6894432 | biostudies-literature
Project description:We analyzed the transcriptomic profiles Pepck-Vpr mouse kidney by single-nuclear RNA-seq.
2024-06-12 | GSE223777 | GEO
Project description:The specificity of gene activation, both the dCasMINI-VPR and dhpCasMINI-VPR significantly and obviously activated IL1RN and only a few genes showed expression change, indicating high genome-wide targeted transcriptional specificity.
2024-06-29 | GSE270586 | GEO
Project description:Construction of ceRNA network based on an RNA‑seq shows prognostic lncRNA biomarkers in Perthes’ disease
| PRJNA901386 | ENA
Project description:Lentiviral accessory genes enhance replication through diverse mechanisms. HIV-1 accessory protein Vpr modulates the host DNA damage response (DDR) at multiple steps through DNA damage, cell cycle arrest, the degradation of host proteins, and both the activation and repression of DDR signaling. Vpr also alters host and viral transcription; however, the connection between Vpr-mediated DDR modulation and transcriptional activation remains unclear. Here, we determined the cellular consequences of Vpr-induced DNA damage using Vpr mutants that allow us to separate the ability of Vpr to induce DNA damage from cell cycle arrest and other DDR phenotypes including host protein degradation and repression of DDR. RNA-sequencing of cells expressing Vpr or Vpr mutants identified that Vpr alters cellular transcription through mechanisms both dependent and independent of cell cycle arrest. In tissue-cultured U2OS cells and primary human monocyte-derived macrophages (MDMs), Vpr-induced DNA damage activates the ATM-NEMO pathway and alters cellular transcription via NF-κB/RelA signaling. HIV-1 infection of primary MDMs validated Vpr-dependent NF-κB transcriptional activation during infection. Both virion delivered and de novo expressed Vpr induced DNA damage and activated ATM-NEMO dependent NF-κB transcription, suggesting that engagement of the DDR and transcriptional reprogramming can occur during early and late stages of viral replication. Together, our data identifies a mechanism by which Vpr activates NF-κB through DNA damage and the ATM-NEMO pathway, which occur independent of cell cycle arrest. We propose this is essential to overcoming restrictive environments, such as in macrophages, to enhance viral transcription and replication.
2024-08-23 | GSE253779 | GEO