Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Isoginkgetin induces autophagic cell death in hepatocellular carcinoma [ChIP-seq 2]

ABSTRACT: Purpose: Our previous studies have identified isoginkgetin as an inducer of autophagic cell death in hepatocellular carcinoma. We set out to analyze how isoginkgetin regulates the genome-wide enhancer activity in HepG2 cells. Methods: ChIP-seqs for H3K4me, H4K8ac, H3K27me3 and H3K9ac were performed in HepG2 followed by treatment with 20 μM isoginkgetin for 24 h. Conclusions: Isoginkgetin treatment reduces the expression of glucose transporters and inhibts SLC2A1 enhancer activity in HepG2 cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE202612 | GEO | 2023/03/22

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Isoginkgetin induces autophagic cell death in hepatocellular carcinoma [ChIP-Seq]

Project description:Purpose: Our previous studies have identified isoginkgetin as an inducer of autophagic cell death in hepatocellular carcinoma. We set out to analyze how isoginkgetin regulates the genome-wide enhancer activity in HepG2 cells. Methods: ChIP-seq for H3K27ac was performed in HepG2 followed by treatment with 20 μM isoginkgetin for 24 h. Conclusions: Isoginkgetin treatment reduces the expression of glucose transporters and inhibts SLC2A1 enhancer activity in HepG2 cells.

2023-03-22 | GSE188534 | GEO

Isoginkgetin induces autophagic cell death in hepatocellular carcinoma [RNA-Seq]

Project description:Purpose: Our previous studies have identified Isoginkgetin as an inducer of autophagic cell death in hepatocellular carcinoma. We set out to analyze how isoginkgetin regulates gene expression in HepG2 cells. Methods: RNA-seq was performed with two repetitions in HepG2 followed by treatment with DMSO and 20 μM Isoginkgetin for 24 h. Conclusions: Isoginkgetin treatment reduces the expression of glucose transporters in HepG2 cells.

2023-03-22 | GSE188533 | GEO

A total RNA-Seq screen reveals that the splicing inhibitor Isoginkgetin blocks transcription elongation

Project description:Pharmacological perturbation is a powerful tool for understanding gene expression, but identification of the specific steps of this multi-step process targeted by small molecules remains challenging. Here we apply total RNA-Seq to distinguish specific pharmacological effects on transcription and pre-mRNA processing, revealing unexpectedly that the splicing inhibitor isoginkgetin blocks transcription elongation.An RNA-Seq screen reveals that the compounds TBBz and CYT387 mimic the transcriptional effects of isoginkgetin and are inhibitors of CSNK2A2, suggesting that isoginkgetin blocks transcription elongation via inhibition of CSNK2A2. Our results reveal RNA-Seq screening as a tool for disentangling complex pharmacological effects on gene expression.

2016-09-17 | GSE86857 | GEO

Microarray analysis of isoginkgetin-treated HCT116 and HCT116p53-/- cells

Project description:Microarray analysis of isoginkgetin-treated HCT116 and HCT116p53-/- cells

| PRJNA748989 | ENA

Isoginkgetin induces autophagic cell death in hepatocellular carcinoma

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-03-22 | GSE188535 | GEO

Microarray analysis of isoginkgetin-treated HCT116 and HCT116p53-/- cells

Project description:Isoginkgetin (IGG) is a small molecule inhibitor of the spliceosome although the direct target remains elusive. Widespread failure to accurately remove introns poses a risk to cells and organisms through the potential production of aberrant mRNAs and proteins. The cellular responses to accumulation of these intermediates and/or the direct interference of spliceosome assembly itself may constitute a splicing stress but this is not well defined yet. We used oligonucleotide microarrays to assess genome wide changes in gene expression associated with exposure to IGG in HCT116 cells and an isogenic subline lacking the p53 tumor suppressor that responds to a variety of transcriptional stresses (Oncogene 18 (3), 583-592). Two of the 3 enriched pathways identified using PANTHER analysis of differentially expressed transcripts are linked to the ATF4 transcription factor and these effects are p53-independent.

2021-07-23 | GSE180623 | GEO

Liver gene expression analysis of male ApoE-/- mice treated with Isoginkgetin

Project description:Isoginkgetin (ISOGK) is a biflavone derived from Ginkgo Biloba that inhibits RNA splicing. ISOGK has been reported to have various protective effects, including anti-inflammatory, antioxidant, and anti-tumorigenic properties. The study aimed to investigate the impact of ISOGK treatment on atherosclerosis induced by a Western diet in ApoE-/- mice. After seven weeks of a high-fat diet, ISOGK was administered intraperitoneally for eight weeks. At the endpoint, mice were euthanized for sample collection, and a series of indicators were tested. The study results indicate that the ISOGK treatment group significantly reduced the area of aortic plaques, aortic sinus plaques, and the necrotic core area. Additionally, ISOGK significantly lowered the levels of total cholesterol in the serum. These findings suggest that ISOGK is effective in treating atherosclerosis and reducing blood lipid levels.

2024-05-15 | GSE261858 | GEO

Miz1 is required to maintain autophagic flux

Project description:Miz1 is required to maintain autophagic flux

| PRJNA210788 | ENA

Isoginkgetin derivative IP2 enhances the adaptive immune response against tumor antigens

Project description:The success of cancer immunotherapy relies on the induction of an immunoprotective response targeting tumor antigens (TAs) presented on MHC-I molecules. We demonstrated that the splicing inhibitor isoginkgetin and its water-soluble and non-toxic derivative IP2 act at the production stage of the Pioneer Translation Products (PTPs). We showed that IP2 increases PTP-derived antigen presentation in cancer cells in vitro and impairs tumor growth in vivo. IP2 action is long-lasting and dependent on the CD8+ T cell response against TAs. We observed that the antigen repertoire displayed on MHC-I molecules at the surface of MCA205 fibrosarcoma is modified upon treatment with IP2. In particular, IP2 enhances the presentation of an exon-derived epitope from the tumor suppressor nischarin. The combination of IP2 with a peptide vaccine targeting the nischarin-derived epitope showed a synergistic antitumor effect. These findings identify the spliceosome as a druggable target for the development of epitope-based immunotherapies.

2021-03-02 | PXD023019 | Pride

Unraveling autophagic imbalances and therapeutic insights in Mecp2-deficient models

Project description:Loss of function mutations in MECP2are associated to Rett syndrome (RTT), a severe neurodevelopmental disease. Mainly working as a transcriptional regulator, MECP2 absence leads to gene expression perturbations resulting in deficits of synaptic function and neuronal activity. In addition, RTT patients and mouse models suffer from a complex metabolic syndrome, suggesting that related cellular pathways might contribute to neuropathogenesis. Along this line, autophagy is critical in sustaining developing neuron homeostasis by breaking down dysfunctional proteins, lipids, and organelles. Here, we investigated the autophagic pathway in RTT and found reduced content of autophagic vacuoles in Mecp2 knock-out neurons. This correlates with defective lipidation of LC3B-II probably caused by a deficiency of the autophagic membrane lipid phosphatidylethanolamine. The administration of the autophagy inducer trehalose recovers LC3B lipidation, autophagosomes content in knock-out neurons, and ameliorates their morphology, neuronal activity and synaptic ultrastructure. Moreover, we provide evidence for attenuation of motor and exploratory impairment in Mecp2 knock-out mice upon trehalose administration. Overall, our findings open new perspectives for neurodevelopmental disorders therapies based on the concept of autophagy modulation.

2024-08-26 | GSE271893 | GEO

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