Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptomic study of PIK3D transfected-Huh7 cells

ABSTRACT: The isoform delta of class I Phosphoinositide 3-kinase (PI3Kδ) is expressed primarily in hematopoietic cells, and its inhibitor, idelalisib, is approved for the treatment of leukemia and lymphoma. PI3K orients the apicobasal axis and regulates lumen formation through assembly of the extracellular matrix. PI3Kδ overexpression in hepatocellular carcinoma (HCC) cells (Huh7) leads to profound changes in cell morphogenesis and is associated to the up-regulation of stem cell markers. Transcriptomic analysis performed in triplicate on mRNA of Huh7 cells transfected with PI3Kδ construct (PI3KCD) revealed down regulation of transcripts of hepatocyte differentiation genes and up regulation of transcripts that allow prediction of ICC and mesenchymal stem cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE128022 | GEO | 2020/11/30

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Transcriptomic study with knock-in of PIK3CD in tumoral experimental mouse model

Project description:The isoform delta of class I Phosphoinositide 3-kinase (PI3Kdelta) is expressed primarily in hematopoietic cells, and its inhibitor, idelalisib, is approved for the treatment of leukemia and lymphoma. PI3Kdelta orients the apicobasal axis and regulates lumen formation through assembly of the extracellular matrix. PI3Kdelta overexpression in hepatocellular carcinoma (HCC) cells (Huh7) leads to profound changes in cell morphogenesis and is associated to the up-regulation of stem cell markers. With tumoral experimental mouse model, investigations on PI3Kdelta implication were performed after knock-in transfection

2021-09-05 | GSE183392 | GEO

PI3Kδ inhibition potentiates glucocorticoids in B-ALL by decreased receptor phosphorylation and enhanced gene regulation

Project description:Glucocorticoids, including dexamethasone and prednisone, are key components of therapy for B-lymphoblastic leukemia (B-ALL) that work through the glucocorticoid receptor (GR). However, glucocorticoids are not effective for all patients, leading to poor outcomes, and the high doses used in chemotherapy cause many toxicities. We have shown that inhibition of the leukocyte restricted PIK3δ is a promising way to specifically enhance glucocorticoids in B-ALL, with the potential to improve outcomes without increasing toxicities. Here, we show that the PI3Kδ inhibitor idelalisib potentiates both prednisolone and dexamethasone in both B-ALL cell lines and primary patient specimens, particularly at sub-saturating doses. Potentiation is partially explained by a widespread enhancement of glucocorticoid gene regulation, including effector genes that drive B-ALL cell death. Idelalisib causes a reduction in direct phosphorylation of GR at S203 and S226. Ablation of these phospho-acceptor sites enhances glucocorticoid potency. Phosphorylation of S226 inhibits GR DNA binding, indicating that PI3Kδ mediated phosphorylation directly inhibits GR function in part though reduction of DNA binding affinity. Thus, PI3Kδ inhibition improves glucocorticoid efficacy in B-ALL in part by decreasing GR phosphorylation and enhancing DNA binding and downstream gene regulation. Identification of this and other contributing mechanisms will help identify patients who can most benefit clinically from this combination therapy.

2022-10-18 | GSE215385 | GEO

Phosphatidylinositol 3-Kinase (PI3K) delta blockade increases genomic instability in B cells

Project description:Activation-induced cytidine deaminase (AID) is a B-cell specific enzyme that targets immunoglobulin (Ig) genes to initiate class switch recombination (CSR) and somatic hypermutation (SHM). Through off-target activity, however, AID has a much broader impact on genomic instability by initiating oncogenic chromosomal translocations and mutations involved in lymphoma development and progression. AID expression is tightly regulated in B cells and its overexpression leads to enhanced genomic instability and lymphoma formation. The phosphatidylinositol 3-kinase (PI3K) δ pathway plays a key role in AID regulation by suppressing its expression in B cells. Novel drugs for leukemia or lymphoma therapy such as idelalisib, duvelisib or ibrutinib inhibit PI3Kδ activity directly or indirectly through inhibition of the Bruton tyrosine kinase (BTK), thus possibly affecting AID expression and, consequently, genomic stability in B cells. Here we show that treatment of primary mouse B cells with idelalisib or duvelisib, and to a lesser extent ibrutinib, enhanced the expression of AID and increased somatic hypermutation (SHM) and chromosomal translocation frequency to the Igh locus and to several AID off-target sites. These effects were both completely abrogated in AID deficient B cells. PI3Kδ inhibitors or ibrutinib increased the formation of AID-dependent tumors in pristane-treated mice. Consistently, PI3Kδ inhibitors enhanced AID expression and translocation frequency to IgH and AID off-target sites in human chronic lymphocytic leukemia (CLL) and mantle cell lymphoma (MCL) cell lines, and patients treated with idelalisib showed increased SHM in AID off-targets. In summary, we show that PI3Kδ or BTK inhibitors increase genomic instability in normal and neoplastic B cells by an AID-dependent mechanism. Since such inhibitors are administered for years to patients, their genotoxic potential should be carefully considered while planning therapeutic protocols.

2017-01-31 | GSE77788 | GEO

DNA microarray analysis of Huh7 and JMJD5KO Huh7 cells.

Project description:To understand the roles of JMJD5 in liver cells, we performed DNA microarray analysis by using JMJD5KO Huh7 cells. We noticed that several transcriptional factors involved in differentiation to hepatocytes were down-regulated in JMJD5KO Huh7 cells compared to parent Huh7 cells..

2016-01-23 | GSE73491 | GEO

Hepatocellular carcinoma Huh7: siHINT1 vs. siControl

Project description:LncRNA and mRNA expression profiling of Hepatocellular carcinoma Huh7 when HINT1 knockdown. HINT1 is a novel tumor suppressor gene, which can regulate the transcription of a variety of cancer-related genes, and its regulation networks is poorly understood in hepatocellular carcinoma. We used the total RNA from siControl and siHINT1 Huh7 cells to analyze the differentially expressed lncRNA and mRNA which were regulated by HINT1, and further explored the ceRNA network that HINT1 may involved.

2022-03-09 | GSE177624 | GEO

Expression profile in Huh7 cell treated with KRT19 shRNA

Project description:We aimed to investigate the involvement of genes in the down-regulation of KRT19 in Huh7 cell lines. Stably knocked down KRT-19 in Huh7, the corresponding empty plasmid of PLL3.7 treated control cells were applied to extract the total RNA from three samples in each group, and were amplified and transcribed into fluorescent complementary DNA (cDNA). Labeled samples were hybridized to the Human Roche NimbleGen mRNA microarray (Roche, Basel, Switzerland).

2015-01-19 | E-MTAB-2559 | biostudies-arrayexpress

Expression Profiling in Selenite-induced Proliferation of HuH7 cells

Project description:Experimental studies confirmed that seleium induced a global change of gene expression in HuH7 cells. Several novally induced secretory growth factors may contribute to the autocrine mode of growth elicited by selenium treatment. Keywords: Treatment HuH7 were cultured in 0.1 Î¼M sodium selenite-containing medium for 15 passages (SELT) or in serum-free medium for 30 h (SF30) or in the regular complete medium containing 10 % fetal calf serum (HUH7) for 30 h. The total RNA were reverse transcried and hybridized to Human 8K-1 (Egenomix Technology Corp., Taiwan). The hybridization time and temperature was 16 h and 62â??, respectively. SELT and HUH7 samples were labeled with Cy5 while SF30 sample was labeled with Cy3. Local background correction and interchip global normalization were accomplished by GenePix Pro 5.0 (Molecular Devices, Sunnyvale, CA ). Genes with differential up- or down-regulation by 1.5 fold with respect to the SF30 cells were obtained using GeneSpring software 7.0 (Silicon Genetics, Agilent Technologies).

2010-06-30 | E-GEOD-4593 | biostudies-arrayexpress

The PI3Kδ interactome in naïve and activated mouse CD4+ T cells

Project description:Phosphoinositide 3-kinases (PI3Ks) play a central role in adaptive immunity by transducing signals from the T cell antigen receptor (TCR) via production of PIP3. PI3Kδ is a heterodimer composed of a p110δ catalytic subunit associated with a p85α or p85β regulatory subunit and is preferentially engaged by the TCR upon T cell activation. The molecular mechanisms leading to PI3Kδ recruitment and activation at the TCR signalosome remain unclear. In this study, we have used affinity purification coupled with quantitative mass spectrometry to uncover the p110δ interactome in primary CD4+ T cells. Moreover, we have determined how the PI3Kδ interactome changes upon the differentiation of small naïve T cells into T cell blasts expanded in the presence of IL-2.

2021-03-08 | PXD022607 | Pride

Effect of depletion of METTL16 on gene expression of Huh7 liver cancer cells [RNA-seq]

Project description:To investigate the mechanism of METTL16 in the regulation of tranlation and HCC development, we established Huh7 cell lines following METTL16 knockout (KO) by CRISPER-Cas9 system. We then performed gene expression profiling analysis using data obtained from RNA-seq of Huh7 cells.

2024-01-30 | GSE224008 | GEO

RNA seq data of Hep3B-control, Hep3B-sertraline, Hep3B-XL413, Hep3B-XL413-sertraline, Huh7-control, Huh7-sertraline, Huh7-XL413, Huh7-XL413-sertraline cells

Project description:RNA seq data of Hep3B-control, Hep3B-sertraline, Hep3B-XL413, Hep3B-XL413-sertraline, Huh7-control, Huh7-sertraline, Huh7-XL413, Huh7-XL413-sertraline cells

| PRJNA496576 | ENA

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data