Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

MATR3 Promotes Liver Cancer Progression by Suppressing DHX58–Mediated Type I Interferon Response

ABSTRACT: MATR3 Promotes Liver Cancer Progression by Suppressing DHX58–Mediated Type I Interferon Response

PROVIDER: PRJNA1102298 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other
	SRR28743371_1.fastq.gz	Fastqsanger.gz
	SRR28743371_2.fastq.gz	Fastqsanger.gz

Items per page:

1 - 3 of 3

Similar Datasets

MATR3 Promotes Liver Cancer Progression by Suppressing DHX58–Mediated Type I Interferon Response

Project description:To investigate the mechanism of Matr3 in liver cancer, we stably knocked out Matr3 in Hepa1-6 cells and performed RNA sequencing with wild-type Hepa1-6 cells

2025-04-01 | GSE264380 | GEO

Pre-treatment of Interferon-α stimulates DHX58 to prevent hepatic ferroptosis [DHX58 RIP-Seq]

Project description:Characterized by lethal iron accumulation and lipid peroxidation, ferroptosis plays critical roles in liver injury, especially caused by ischemia/reperfusion (I/R) of hepatic inflow occlusion during liver operation. Here, we found that the excessive production of reactive oxygen species could decrease the expression of Interferon (IFN)-stimulated gene DExH-box helicase 58 (DHX58) in hepatocytes, and then promote hepatic ferroptosis, while pre-treatment using IFN-α increased DHX58 expression and prevented ferroptosis during I/R injury. Mechanistically, DHX58 with RNA-binding activity could constitutively associate the mRNA of glutathione peroxidase 4 (GPX4), a crucial ferroptosis suppressor, and then recruit the m6A reader YT521-B homology domain containing 2 (YTHDC2) to promote the translation of Gpx4 mRNA in m6A-dependent manner, thus enhancing GPX4 protein level and preventing hepatic ferroptosis.

2025-04-28 | GSE231843 | GEO

Pre-treatment of Interferon-α stimulates DHX58 to prevent hepatic ferroptosis

Project description:Characterized by lethal iron accumulation and lipid peroxidation, ferroptosis plays critical roles in liver injury, especially caused by ischemia/reperfusion (I/R) of hepatic inflow occlusion during liver operation. However, the lack of effective and safe clinical precautionary measure is still the main problem in preventing hepatic ferroptosis. Here, we found that the excessive production of reactive oxygen species could decrease the expression of Interferon (IFN)-stimulated gene DExH-box helicase 58 (DHX58) in hepatocytes, and then promote hepatic ferroptosis, while pre-treatment using IFN-α increased DHX58 expression and prevented ferroptosis during I/R injury. Mechanistically, DHX58 with RNA-binding activity could constitutively associate the mRNA of glutathione peroxidase 4 (GPX4), a crucial ferroptosis suppressor, and then recruit the m6A reader YT521-B homology domain containing 2 (YTHDC2) to promote the translation of Gpx4 mRNA in m6A-dependent manner, thus enhancing GPX4 protein level and preventing hepatic ferroptosis. Therefore, we provide mechanistic evidence for the IFN-stimulated DHX58 in promoting the translation of m6A-modified Gpx4 mRNA, and suggest the promising clinical potential of IFN-α pre-treatment in the prevention of hepatic ferroptosis.

2024-05-24 | PXD042083 | Pride

Pre-treatment of Interferon-α stimulates DHX58 to prevent hepatic ferroptosis [DHX58 RIP-Seq]

Project description:Pre-treatment of Interferon-α stimulates DHX58 to prevent hepatic ferroptosis [DHX58 RIP-Seq]

| PRJNA968014 | ENA

Pre-treatment of Interferon-α stimulates DHX58 to prevent hepatic ferroptosis [m6A RIP]

2025-04-28 | GSE231842 | GEO

Pre-treatment of Interferon-α stimulates DHX58 to prevent hepatic ferroptosis [scRNA-seq]

2025-04-28 | GSE231934 | GEO

MATR3

Project description:MATR3

| PRJNA823719 | ENA

Pre-treatment of Interferon-α stimulates DHX58 to prevent hepatic ferroptosis