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

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-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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE188534 | GEO | 2023/03/22

REPOSITORIES: GEO

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

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-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.

2023-03-22 | GSE202612 | 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

Isoginkgetin induces autophagic cell death in hepatocellular carcinoma

Project description:Isoginkgetin induces autophagic cell death in hepatocellular carcinoma

| PRJNA779367 | ENA

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

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

| PRJNA779373 | ENA

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

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

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

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

| PRJNA836776 | 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

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

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

Targeting sphingosine kinase by ABC294640 induces KSHV-infected endothelial cell autophagic death

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