Ferroptosis Mediates Zinc Toxicity: Implications for Cancer Therapy

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11110%2F25%3A10498072" target="_blank" >RIV/00216208:11110/25:10498072 - isvavai.cz</a>

Výsledek na webu

<a href="https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=nzs0MkZJCA" target="_blank" >https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=nzs0MkZJCA</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.32604/biocell.2025.063301" target="_blank" >10.32604/biocell.2025.063301</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Ferroptosis Mediates Zinc Toxicity: Implications for Cancer Therapy

Popis výsledku v původním jazyce

Ferroptosis is an iron-driven, phospholipid hydroperoxide-mediated cell death, which has recently emerged as an attractive tool in cancer research due to its ability to govern the anti-tumor immune response. A growing research interest in ferroptosis biology has revealed the contribution of this regulated cell death to multiple diseases. In addition to iron, ferroptosis has been reported to be triggered by multiple heavy metals, which sheds light on the novel aspects of heavy metals-induced cytotoxicity. In this review, the ability of zinc, an essential biogenic element with a wide array of biological functions, to modulate ferroptosis in normal and malignant cells has been summarized. Accumulating evidence suggests that zinc-induced biological effects can be mediated by ferroptosis induction or attenuation. In addition, the anti-cancer effects of zinc can be at least partly attributed to ferroptosis induction. The signaling pathways governing zinc-regulated ferroptosis are highlighted. It has been underscored that zinc-mediated modulation of ferroptosis is dependent on alterations of redox homeostasis, antioxidant defense (in particular, the SLC7A11/GSH/GPX4 axis), and iron metabolism. Additionally, data on ferroptosis induction by zinc oxide nanoparticles are summarized to emphasize the potential of these nanomaterials as a promising therapeutic choice in anti-cancer treatment.

Název v anglickém jazyce

Ferroptosis Mediates Zinc Toxicity: Implications for Cancer Therapy

Popis výsledku anglicky

Ferroptosis is an iron-driven, phospholipid hydroperoxide-mediated cell death, which has recently emerged as an attractive tool in cancer research due to its ability to govern the anti-tumor immune response. A growing research interest in ferroptosis biology has revealed the contribution of this regulated cell death to multiple diseases. In addition to iron, ferroptosis has been reported to be triggered by multiple heavy metals, which sheds light on the novel aspects of heavy metals-induced cytotoxicity. In this review, the ability of zinc, an essential biogenic element with a wide array of biological functions, to modulate ferroptosis in normal and malignant cells has been summarized. Accumulating evidence suggests that zinc-induced biological effects can be mediated by ferroptosis induction or attenuation. In addition, the anti-cancer effects of zinc can be at least partly attributed to ferroptosis induction. The signaling pathways governing zinc-regulated ferroptosis are highlighted. It has been underscored that zinc-mediated modulation of ferroptosis is dependent on alterations of redox homeostasis, antioxidant defense (in particular, the SLC7A11/GSH/GPX4 axis), and iron metabolism. Additionally, data on ferroptosis induction by zinc oxide nanoparticles are summarized to emphasize the potential of these nanomaterials as a promising therapeutic choice in anti-cancer treatment.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

10600 - Biological sciences

Projekt

—

Návaznosti

V - Vyzkumna aktivita podporovana z jinych verejnych zdroju

Rok uplatnění

2025

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Biocell

ISSN

0327-9545

e-ISSN

1667-5746

Svazek periodika

49

Číslo periodika v rámci svazku

5

Stát vydavatele periodika

AR - Argentinská republika

Počet stran výsledku

21

Strana od-do

721-741

Kód UT WoS článku

001454316100001

EID výsledku v databázi Scopus

2-s2.0-105006686682