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Mismanagement of Cellular Iron Leads to Ferroptosis Susceptibility in Cancer Cells Surviving Chemotherapy

ABSTRACT: Mismanagement of Cellular Iron Leads to Ferroptosis Susceptibility in Cancer Cells Surviving Chemotherapy

PROVIDER: PRJNA1196449 | ENA |

REPOSITORIES: ENA

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Mismanagement of Cellular Iron Leads to Ferroptosis Susceptibility in Cancer Cells Surviving Chemotherapy

Project description:Despite centuries of research, metastatic cancer remains incurable due to resistance against all conventional cancer therapeutics. Alternative strategies leveraging non-proliferative vulnerabilities in cancer are required to overcome cancer recurrence. Ferroptosis is an iron dependent cell death pathway that has shown promising pre-clinical activity in several contexts of therapeutic resistant cancer. However, ferroptosis sensitivity is highly variable across tissue types and cell state posing a challenge for clinical translation. We describe a convergent phenotype induced by chemotherapy where cells surviving chemotherapy have similar transcriptomic signatures and dysregulated iron homeostasis, regardless of initial cell type or chemotherapy used. Elevated labile iron levels are counteracted by NRF2 signaling that does not alleviate the amount of labile iron. Selectively inhibiting GPX4 leads to uniform susceptibility to ferroptosis in surviving cells, highlighting the common reliance on lipid peroxidation defenses. Cellular iron dysregulation is a vulnerability of chemoresistant cancer cells that can be leveraged by triggering ferroptosis

2025-05-19 | GSE297299 | GEO

Mismanagement of Cellular Iron Leads to Ferroptosis Susceptibility in Cancer Cells Surviving Chemotherapy

2025-05-13 | GSE283982 | GEO

Mismanagement of Cellular Iron Leads to Ferroptosis Susceptibility in Cancer Cells Surviving Chemotherapy

Project description:Mismanagement of Cellular Iron Leads to Ferroptosis Susceptibility in Cancer Cells Surviving Chemotherapy

| PRJNA1263486 | ENA

PD-L1 regulates dendritic cell ferroptosis during immunogenic chemotherapy

Project description:PD-L1 regulates dendritic cell ferroptosis during immunogenic chemotherapy

| PRJNA876931 | ENA

Sub-lethal stimulation of ferroptosis leads to trophoblast dysfunction

Project description:Sub-lethal stimulation of ferroptosis leads to trophoblast dysfunction

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Sub-lethal stimulation of ferroptosis leads to trophoblast dysfunction

Project description:Ferroptosis is a recently identified program of regulated cell death, defined by excessive accumulation of hydroperoxy-arachidonoyl (C20:4)- or adrenoyl (C22:4)- phosphatidyl-ethanolamine (OOH-PE). The selenium-dependent glutathione peroxidase 4 (GPX4) inhibits ferroptosis, converting unstable ferroptotic lipid hydroperoxides to non-toxic lipid alcohols. The effect of GPX4 ablation is divergent among cells and tissues, suggesting that additional regulators may guard trophoblasts against ferroptosis. While placental oxidative stress and lipotoxicity are hallmarks of placental dysfunction, the possible role of ferroptosis in placental function has not been hitherto investigated. Here we found that placental dysfunction is associated with ferroptosis, and that inhibition of GPX4 causes trophoblast injury and ferroptosis in vitro and in vivo during mouse pregnancy. Importantly, we uncover a role for the phospholipase PLA2G6 (PNPLA9, iPLA2beta), known to metabolizes OOH-PE to lyso-PE and oxidized fatty acid, in mitigating ferroptosis induced by GPX4 inhibition in vitro or by hypoxia-reoxygenation injury in vivo. Together, we identified ferroptosis in the human and mouse placenta, and established a novel role for PLA2G6 in attenuating trophoblastic ferroptosis. Our data provide mechanistic insights to the ill-defined entity of placental lipotoxicity, and may inspire new therapeutic strategies that target PLA2G6 as a means to modulate ferroptosis in placental and non-placental tissue.

2020-09-27 | GSE147625 | GEO

Plasticity of ether lipids promotes ferroptosis susceptibility and evasion

Project description:Ferroptosis, an iron-dependent, non-apoptotic cell death program, is involved in a variety of degenerative diseases and represents a targetable vulnerability in certain cancers. The ferroptosis-susceptible cell-state can either preexist in cells arising from certain lineages or be acquired during cell-state transitions. Precisely how ferroptosis susceptibility is dynamically regulated remains poorly understood. Using genome-wide CRISPR/Cas9 suppressor screens, we identify a key role for peroxisome–ether phospholipid genes in driving ferroptosis susceptibility and evasion in ovarian cancer.

2020-09-16 | GSE151062 | GEO

Fasting-mimicking diet synergizes with ferroptosis against quiescent, chemotherapy-resistant cells

Project description:Fasting-mimicking diet synergizes with ferroptosis against quiescent, chemotherapy-resistant cells

| PRJNA885828 | ENA

PD-L1 regulates dendritic cell ferroptosis during immunogenic chemotherapy [scRNA-seq]

Project description:PD-L1 regulates dendritic cell ferroptosis during immunogenic chemotherapy [scRNA-seq]

| PRJNA926616 | ENA

NANS suppresses NF-κB signaling to promote ferroptosis by perturbing iron homeostasis

Project description:During metastasis, cancer cells face significant survival pressures, including treatment-induced ferroptosis. Adaptation to ferroptosis stress orchestrates the metastasis of colorectal cancer (CRC) cells. However, the reciprocal regulatory mechanisms of ferroptosis and metastasis remain unknown. Here, through a CRISPR–Cas9 screen, we discovered that N-acetylneuraminate synthase (NANS) is a positive regulator of ferroptosis in CRC, regardless of its metabolic function. Moreover, NANS expression is downregulated and is clinically associated with poor prognosis in CRC patients. In a ferroptotic stress environment, NANS is phosphorylated by cyclin-dependent kinase 1 (CDK1) at serine 275 (S275), and phosphorylated NANS (NANS pS275) dissociates from TAK1 and is subsequently ubiquitinated by the E3 ligase ubiquitin-conjugating enzyme E2 N (UBE2N) at lysine 246 (K246) for degradation, which further activates TAK1 and nuclear factor κB (NF-κB) signaling and the expression of the ferroptosis negative regulatory factor FTH1, resulting in ferroptosis resistance and finally promoting metastasis. Furthermore, the NANS pS275 intensity is correlated with the degree of malignancy and the prognosis of CRC patients. Our study revealed that NANS inhibits CRC metastasis by promoting ferroptosis and that the CDK1-mediated phosphorylation of NANS at S275 may guide the utilization of chemical compounds to promote ferroptosis and thus block CRC metastasis.

2025-05-08 | PXD062501 | Pride

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