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Next Generation Sequencing Facilitates Quantitative Analysis of HCC Cell Line HepG2 Cells with Inhibited P2X7 Receptor Signaling by Antagonist A740003 or A438079

ABSTRACT: The goals of this study aim to reveal the role of P2X7 receptor signaling in HCC

ORGANISM(S): Homo sapiens

PROVIDER: GSE268508 | GEO | 2024/11/27

REPOSITORIES: GEO

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Next Generation Sequencing Facilitates Quantitative Analysis of HCC Cell Line HepG2 Cells with Inhibited P2X7 Receptor Signaling by Antagonist A740003 or A438079

Project description:Next Generation Sequencing Facilitates Quantitative Analysis of HCC Cell Line HepG2 Cells with Inhibited P2X7 Receptor Signaling by Antagonist A740003 or A438079

| PRJNA1117474 | ENA

Next Generation Sequencing Facilitates Quantitative Analysis of DLBCL Cell Line SU-DHL-4 Cells with P2X7 Receptor Signaling Activation or Inhibition

Project description:The goals of this study aim to reveal the role of P2X7 receptor signaling in DLBCL

2023-07-12 | GSE225174 | GEO

Gene expression profile of Wild Type (WT) and P2x7 knockout (P2X7-KO) leukemia leukemia-initiating cells Transcriptomes

Project description:To determine the underlying molecular mechanisms that control the homing and self-renewal activities of P2x7-null Mac-1+c-Kit+ LICs, WT and P2x7-null LICs were WT and P2x7-KO were sorted by flow cytometry, followed by the extraction of total RNA and subjected to the RNA-sequencing.

2023-11-30 | GSE162468 | GEO

Next Generation Sequencing Facilitates Quantitative Analysis of Wild Type HCC cells with or without RNase7 treatment, and FIG-ROS1 Fusion Transcriptomes

Project description:The goals of this study are to compare RNase7-induced or fusion-driven HCC cell transcriptome profiling

2022-12-31 | GSE156510 | GEO

The ATP-P2X7 signaling axis is dispensable for obesity-associated inflammasome activation in adipose tissue

Project description:Inflammasome activation in adipose tissue has been implicated in obesity-associated insulin resistance and type 2 diabetes. However, when and how inflammasome is activated in adipose tissue remains speculative. Here we test the hypothesis that extracellular ATP, a potent stimulus of inflammasome in macrophages via purinergic receptor P2X, ligand-gated ion channel, 7 (P2X7), may play a role in inflammasome activation in adipose tissue in obesity. Our data show that inflammasome is activated in adipose tissue upon 8-week feeding of 60% HFD, coinciding with the onset of hyperglycemia and hyperinsulinemia as well as the induction of P2X7 in adipose tissue. Unexpectedly, P2X7-deficient animals on HFD exhibit no changes in metabolic phenotypes, nor in inflammatory responses or inflammasome activation when compared to the wildtype controls. Similar observations have been obtained in hematopoietic cell-specific P2X7-deficient animals generated by bone marrow transplantation. Thus, we conclude that inflammasome activation in adipose tissue in obesity coincides with the onset of hyperglycemia and hyperinsulinemia, but unexpectedly, is not mediated by the ATP-P2X7 signaling axis. The nature of the inflammasome-activating danger signal(s) in adipose tissue in obesity remains to be characterized. Wild type and P2X7 knockout mice were fed a low fat diet (chow) or high fat diet for 12 weeks. After the diet intervention period, the animals were killed and epididymal white adipose tissue was removed. Total RNA was isolated and subjected to gene expression profiling.

2012-02-24 | E-GEOD-36033 | biostudies-arrayexpress

Next Generation Sequencing Facilitates Quantitative Analysis of Mock- and Hydrogen peroxide (H2O2)-Treated Human Hepatocellular Carcinoma (HCC) Cell Transcriptomes

Project description:Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to compare NGS-derived H2O2-treated HCC transcriptome profiling (RNA-seq) to NGS-derived mock-treated HCC transcriptome profiling. Methods: HCC mRNA profiles of mock-treated Huh7 cells and H2O2-treated Huh7 cells were generated by deep sequencing, in duplicate, using Illumina Pipeline (CASAVA) v1.8.2. The sequence reads that passed quality filters were analyzed at the transcript isoform level with TopHat followed by Cufflinks. qRT–PCR validation was performed using TaqMan and SYBR Green assays Results: RNA-seq data validated with qRT–PCR. RNA-seq data had a linear relationship with qRT–PCR for more than four orders of magnitude and a goodness of fit (R2) of 0.90. Conclusions: We conclude that our study represents the first detailed analysis of H2O2-treated HCC cells transcriptomes compared to mocke-treated HCC cells, with biologic replicates, generated by RNA-seq technology.

2021-01-30 | GSE109915 | GEO

P2X7 receptor-dependent microRNA expression profile in the brain following status epilepticus in mice

Project description:We explored the microRNA expression profile in mice lacking the P2X7 receptor before and after seizures. Genome-wide microRNA profiling was performed using hippocampi from wild-type and P2X7 knock-out mice following status epilepticus induced by intraamygdala kainic acid. This revealed that genetic deletion of the P2X7 receptor results in distinct patterns of microRNA expression. Specifically, we found that in vehicle-injected control mice the lack of P2X7 resulted in the up-regulation of 50 microRNAs and down-regulation of 35 microRNAs. Post-status epilepticus, P2X7 deficiency let to the up-regulation of 44 microRNAs while 13 microRNAs were down-regulated. Moreover, there was only limited overlap between identified P2X7-dependent microRNAs between control conditions and post-status epilepticus, suggesting P2X7 regulating the expression of different microRNAs during normal physiology and pathology. Bioinformatics analysis found that genes targeted via P2X7-dependent microRNAs were particularly overrepresented within pathways involved in intracellular signalling, inflammation and cell death, processes repeatedly linked to P2X7. Moreover, whereas genes involved in signalling pathways and inflammation were common among up-and down-regulated P2X7-dependent miRNAs during physiological and pathological conditions, genes associated with cell death seemed to be restricted to up-regulated miRNAs during both physiological conditions and post-status epilepticus. Taken together, our results demonstrate that P2X7 impacts on the expression profile of microRNAs in the brain, thereby possibly contributing to both the maintenance of normal cellular homeostasis and pathological processes.

2020-06-25 | GSE153204 | GEO

Next Generation Sequencing Facilitates Quantitative Analysis of HCC cells transfected with NCsiRNA or CDCA8siRNA

Project description:We hypothesized if targeting of CDCA8 with small interfering (si) RNA could inhibit HCC progression. We also investigated molecular mechanism to mediate HCC cell death caused by CDCA8 silencing. To accomplish this, Huh1 and Huh7 human HCC cells were transfected with CDCA8 siRNA and tested for growth inhibition and apoptotic induction using MTS, FACS and microscopic analysis. To obtain insights into the molecular changes in response to CDCA8 knockdown, global changes in gene expression were examined using RNA sequencing. As results, siRNA silencing of CDCA8 inhibited HCC cell growth by blocking cell-cycle progression and inducing apoptosis. RNA sequencing showed that, representatively, the anti-proliferative effects were driven by a subset of molecular alterations including the upregulation of tumor suppressive ATF3 and GADD34 genes, whereas a key regulator of cell growth and invasiveness BGLAP was repressed. Subsequent Western blotting also revealed that CDCA8 silencing decreases the levels of pro-caspase 3 and PARP-1, accelerating apoptotic signaling in HCC cells. In addition, targeting CDCA8 effectively suppressed HCC tumor growth growth in a murine xenograft model. Taken together, these findings suggest that CDCA8 could be a promising molecular target for systemic therapy of HCC.

2017-02-14 | GSE77992 | GEO

Next Generation Sequencing Facilitates Quantitative Analysis of HCC cells transfected with NCsiRNA or ODC1siRNA

Project description:We investigated if targeting of ODC1 with siRNA could inhibit HCC progression. To accomplish this, Huh1 and Huh7 human HCC cells were transfected with ODC1 siRNA and tested for growth inhibition and apoptotic induction using MTS, FACS and microscopic analysis. To obtain insights into the molecular changes in response to ODC1 knockdown, global changes in gene expression were examined using RNA sequencing. Our results show that ODC1 silencing caused inhibition of HCC cell growth through blockade of cell cycle progression and a strong induction of apoptosis. Subsequent Western blotting revealed that ODC1 silencing decreased the levels of cell cycle regulator cyclin E1, PARP-1, and pro-caspase 3 accelerating apoptotic signaling in HCC cells. In addition, ODC1 silencing resulted in a strong inhibition in the expressions of important regulators of glycolysis and lipogenesis, GLUT4 and ChREBP, and caused a marked decrease in fat accumulation. These findings suggest that ODC1 can be a promising target for systemic therapy of HCC by modulating tumor metabolism.

2016-12-31 | GSE73268 | GEO

Gene expression changes in wide-type P2X7 overexpressed MLL-AF9 induced mouse acute myeloid leukemia (AML)

Project description:P2X7 was significantly up-regulated in leukemia patients, especially in AML (MLL-AF9) and often related to poor prognosis.We compared the transcriptomic changes in MLL-AF9 induced mouse AML and overexpressed wP2X7 in MLL-AF9 induced AML. Engaged to explore the mechanism of P2X7 in leukemia progression. Mouse AML was induced by expressing MLL-AF9 in mouse HSPCs. Leukemia cells were divided into two groups, c-kit+ and c-kit-. Due to leukemia cells were nearly 95% c-kit+ in P2X7-overexpressed AML cells, we set up four groups of leukemia cells, namely leukemia total cells (V total), leukemia c-kit positive cells (V c-kit+), leukemia c-kit negative cells (V c-kit-), overexpressed wide type P2X7 leukemia cells (wP2X7).

2021-12-29 | GSE92969 | GEO

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