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 [RNA-Seq]

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

PROVIDER: PRJNA779373 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR16903018_1.fastq.gz	Fastqsanger.gz
	SRR16903018_2.fastq.gz	Fastqsanger.gz
	SRR16903019_1.fastq.gz	Fastqsanger.gz
	SRR16903019_2.fastq.gz	Fastqsanger.gz
	SRR16903020_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 8

Similar Datasets

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: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 [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 [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 [ChIP-Seq]

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

| PRJNA779372 | ENA

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

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

Project description:KSHV is a principal causative agent of Kaposi's Sarcoma (KS). Despite this knowledge about the close relationship between sphingolipid metablism and solid tumors development, the role of sphingolipid metablism in KSHV-related malignancies remains mostly unclear. We report that targeting sphingosine kinase 2 (SphK2) by a selective inhibitor, ABC294640, significantly induces KSHV+ TIVE-LTC autophagic death. By using microarray analysis, we have identified the global gene profile affected by ABC294640 within KSHV+ TIVE-LTC and several novel “druggable” candidates closely related to cancer cell survival/growth. Finally, we found that targeting TIVE-LTC by ABC294640 effectively suppressed KSHV tumorigenicity by using a KS-like nude mice model.

2016-11-01 | GSE74338 | GEO

Repurposing amiodarone as a targeted SIRT3 activator that induces autophagic/mitophagic cell death in acute myelocytic leukemia

Project description:Repurposing amiodarone as a targeted SIRT3 activator that induces autophagic/mitophagic cell death in acute myelocytic leukemia

| PRJNA1064069 | ENA

Lapatinib induces autophagic cell death and inhibits growth of human hepatocellular carcinoma.

Project description:Lapatinib, an orally administered small-molecule tyrosine kinase inhibitor targeting epidermal growth factor receptors (EGFR) and Her2/Neu, has been widely accepted in the treatment of breast cancer. In this study, we found that lapatinib induced cytotoxicity in human hepatoma Huh7, HepG2 and HA22T cells. For the mode of cell death, we found lapatinib induced a higher percent of dead cells and a lower percent of hypodiploid cells, suggesting non-apoptotic cell death in lapatinib-treated hepatoma cells. Moreover, lapatinib-induced autophagy in hepatoma cells was confirmed by the detection of autophagic LC3-II conversion, the up-regulation of autophagy-related proteins, and the down-regulation of p62 by immunoblotting. Autophagic cell death was demonstrated by images of punctuated LC3 patterns, a higher percent of acridine orange positive cells, as well as a partial rescue of cell death by autophagy inhibitor 3-methyladenine or chloroquine. We also found massive vacuoles in lapatinib-treated hepatoma cells by electronic microscopy. In addition, the shRNA of knocked-down autophagy-related proteins rescued the hepatoma cells from lapatinib-induced growth inhibition. We also demonstrated a reduction of tumorigenesis by lapatinib in vivo. In conclusion, lapatinib induced autophagic cell death and the growth of human hepatoma cells. Our study provides potential cancer therapies by using lapatinib as a treatment for hepatoma.

| S-EPMC4148104 | biostudies-literature

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

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