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Genome-wide analysis of ferroptosis related genes in liver cancer cells.

ABSTRACT: Genome-wide analysis of ferroptosis related genes in liver cancer cells.

PROVIDER: PRJNA412671 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6122020_1.fastq.gz	Fastqsanger.gz
	SRR6122020_2.fastq.gz	Fastqsanger.gz
	SRR6122021_1.fastq.gz	Fastqsanger.gz
	SRR6122021_2.fastq.gz	Fastqsanger.gz
	SRR6122022_1.fastq.gz	Fastqsanger.gz

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Genome-wide analysis of ferroptosis related genes in liver cancer cells.

Project description:To seek ferroptosis related genes in liver cancer cells, we treated HepG2 cells using ferroptosis inducer Erastin and inhibitor Ferrostatin, respectively. We found that a subset of genes were up-regulated in Erastin treatment groups and down-regulated in Ferrostatin treatment groups, suggesting that these genes might be correlated with ferroptosis.

2019-06-10 | GSE104462 | GEO

A genome-wide CRISPR screen for genes regulating ferroptosis sensitivity

Project description:Genome-wide CRISPR screens were performed in Huh-7 hepatoma cell line to identify genes regulating ferroptosis sensitivity. Huh-7 cells were transduced with Human GeCKO library and selected by RSL-3.

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A genome-wide CRISPR screen for genes regulating ferroptosis sensitivity

Project description:A genome-wide CRISPR screen for genes regulating ferroptosis sensitivity

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Sophoridine derivative 6j inhibits liver cancer cell proliferation via ATF3 mediated ferroptosis

Project description:Liver cancer is one of the most lethal malignancies with an annual death of over 830,000 cases. Although targeted therapeutic drugs have achieved certain clinical efficacy, only sorafenib and lenvatinib are currently marketed as first-line targeted drugs to treat patients with advanced liver cancer. Therefore, developing more drugs are urgently needed. Ferroptosis is an iron-dependent programmed cell death (PCD) distinct from known PCDs including apoptosis, necrosis, and autophagy. Targeting ferroptosis is recognized as a promising potential therapeutic modality for liver cancer. Activating transcription factor 3 (ATF3) is an important ferroptosis inducer and targeting ATF3 offers a potential means to cancer therapy. In the present study, we reported for the first time a sophoridine derivative 6j with promising anti-liver cancer effects in vitro and in vivo. Compound 6j could induce liver cancer cells ferroptosis by promoting the accumulation of intracellular Fe2+, reactive oxygen species (ROS), and MDA. Inhibition of ferroptosis by ferrostatin-1 alleviated 6j induced accumulation of Fe2+, ROS, and MDA and restored cell viability. Further study revealed that compound 6j upregulated the expression of ATF3 via ER stress and knockdown of ATF3 by RNA interference attenuated 6j induced ferroptosis and cell proliferation inhibition. This study would provide new insights for the design of ferroptosis inducers and the development of anti-liver cancer drugs.

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Targeting GPX4-mediated ferroptosis alleviates liver injury in a rat model of intestinal failure-associated liver disease

Project description:Background: Intestinal failure-associated liver disease (IFALD) is a common complication of long-term parenteral nutrition (PN) that is associated with significant morbidity and mortality. Ferroptosis, as an iron-dependent regulated cell death, has been shown to play an important role in the development of several liver diseases. This study focuses on investigating whether the ferroptosis phenomenon is present in TPN-induced IFALD and further exploring the potential regulatory mechanisms. Methods: Ferroptosis hallmarkers were measured in children with short bowel syndrome (SBS) who had long-term PN use and caused IFALD. Sprague-Dawley (SD) rats were used to establish a rat model of IFALD with a concomitant ferroptosis inhibition intervention using liproxstain-1. The mir-431 lineage was identified as a potential upstream regulatory mir-RNA by mir-RNA sequencing. HepG2 and 293T cell line was used to demonstrate that mir-431 regulates ferroptosis through the GPX4 pathway at the cellular level in vitro. Results: Ferroptosis is upregulated in liver of children with IFALD. Liproxstain-1 downregulates ferroptosis in a rat model of IFALD and attenuates hepatic steatosis through the lipid metabolism pathway. In vitro HepG2 and 293T cell experiments reveal that mir-431 affects ferroptosis by regulating GPX4 protein. Conclusions: Ferroptosis plays an important role in the development of IFALD. Liproxstain-1 inhibits ferroptosis and attenuates hepatic steatosis in a rat model of IFALD through the lipid metabolism pathway. Mir-431 negatively regulates GPX4 protein-induced ferroptosis.

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Exploring the phenomenon of ferroptosis in liver disease associated with intestinal failure in children with SBS

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Genome-wide DNA methylation analysis of liver tissue samples obtained from patients with hepatitis virus-related hepatocellular carcinomas

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