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

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

PROVIDER: PRJNA994051 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25246124_1.fastq.gz	Fastqsanger.gz
	SRR25246124_2.fastq.gz	Fastqsanger.gz
	SRR25246125_1.fastq.gz	Fastqsanger.gz
	SRR25246125_2.fastq.gz	Fastqsanger.gz
	SRR25246126_1.fastq.gz	Fastqsanger.gz

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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.

2023-08-23 | GSE237138 | GEO

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

| S-EPMC10425377 | biostudies-literature

ATF3 Inhibits Cardiac Ferroptosis by Directly Binding FANCD2 in Response to Myocardial Ischemia/Reperfusion Injury

Project description:ATF3 Inhibits Cardiac Ferroptosis by Directly Binding FANCD2 in Response to Myocardial Ischemia/Reperfusion Injury

| PRJNA798711 | ENA

ATF3 Inhibits Cardiac Ferroptosis by Directly Binding FANCD2 in Response to Myocardial Ischemia/Reperfusion Injury [ChIP-Seq]

Project description:ATF3 Inhibits Cardiac Ferroptosis by Directly Binding FANCD2 in Response to Myocardial Ischemia/Reperfusion Injury [ChIP-Seq]

| PRJNA798707 | ENA

ATF3 Inhibits Cardiac Ferroptosis by Directly Binding FANCD2 in Response to Myocardial Ischemia/Reperfusion Injury [ChIP-Seq]

Project description:We performed ChIP-seq to find the trageted genes regulated by ATF3 in hypoxia/reoxygenation (H/R)using ATF3 antibody for ChIP.

2023-01-01 | GSE193996 | GEO

ATF3 Inhibits Cardiac Ferroptosis by Directly Binding FANCD2 in Response to Myocardial Ischemia/Reperfusion Injury [RNA-Seq 2]

Project description:ATF3 Inhibits Cardiac Ferroptosis by Directly Binding FANCD2 in Response to Myocardial Ischemia/Reperfusion Injury [RNA-Seq 2]

| PRJNA798716 | ENA

ATF3 Inhibits Cardiac Ferroptosis by Directly Binding FANCD2 in Response to Myocardial Ischemia/Reperfusion Injury [RNA-Seq 1]

Project description:ATF3 Inhibits Cardiac Ferroptosis by Directly Binding FANCD2 in Response to Myocardial Ischemia/Reperfusion Injury [RNA-Seq 1]

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ATF3-activated CBS protects CRC from ferroptosis.

Project description:We performed CUT&Tag to analyze the ATF3 binding gene regulatory element differences.

2022-11-16 | GSE213534 | GEO

Energy-stress-mediated AMPK activation inhibits ferroptosis

Project description:<p>Energy stress depletes ATP and induces cell death. Here we identify an unexpected inhibitory role of energy stress on ferroptosis, a form of regulated cell death induced by iron-dependent lipid peroxidation. We found that ferroptotic cell death and lipid peroxidation can be inhibited by treatments that induce or mimic energy stress. Inactivation of AMP-activated protein kinase (AMPK), a sensor of cellular energy status, largely abolishes the protective effects of energy stress on ferroptosis in vitro and on ferroptosis-associated renal ischaemia-reperfusion injury in vivo. Cancer cells with high basal AMPK activation are resistant to ferroptosis and AMPK inactivation sensitizes these cells to ferroptosis. Functional and lipidomic analyses further link AMPK regulation of ferroptosis to AMPK-mediated phosphorylation of acetyl-CoA carboxylase and polyunsaturated fatty acid biosynthesis. Our study demonstrates that energy stress inhibits ferroptosis partly through AMPK and reveals an unexpected coupling between ferroptosis and AMPK-mediated energy-stress signalling.</p>

2023-01-31 | MTBLS1399 | MetaboLights

ATF3-CBS axis regulates ferroptosis and tumorigenesis via targeting mitochondrial homeostasis

Project description:ATF3-CBS axis regulates ferroptosis and tumorigenesis via targeting mitochondrial homeostasis

| PRJNA881307 | ENA