Abstract
Simple SummaryFerroptosis is a recently defined nonapoptotic form of cell death that is associated with various human diseases, including cancer. As ferroptosis is caused by an overdose of lipid peroxidation resulting from dysregulation of the cellular antioxidant system, it is inherently closely associated with cellular metabolism. Here, we provide an updated review of the recent studies that have shown mechanisms of metabolic regulation of ferroptosis in the context of cancer.Ferroptosis is a unique cell death mechanism that is executed by the excessive accumulation of lipid peroxidation in cells. The relevance of ferroptosis in multiple human diseases such as neurodegeneration, organ damage, and cancer is becoming increasingly evident. As ferroptosis is deeply intertwined with metabolic pathways such as iron, cyst(e)ine, glutathione, and lipid metabolism, a better understanding of how ferroptosis is regulated by these pathways will enable the precise utilization or prevention of ferroptosis for therapeutic uses. In this review, we present an update of the mechanisms underlying diverse metabolic pathways that can regulate ferroptosis in cancer.
Highlights
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An additional mechanism of glutathione peroxidase 4 (GPX4) regulation is by a compound named FIN56 which was identified as a specific inducer of ferroptosis that partially acts by inducing GPX4 degradation [76]
The relevance of ferroptosis in various human diseases have been established, supporting the need for future studies to investigate the role of ferroptosis in these diseases as well as the development of better methods to modulate ferroptosis in vivo
Summary
As the name ‘ferroptosis’ infers, the requirement of intracellular iron is a fundamental property of ferroptosis. As an important trace element in the human body, iron regulates numerous biological processes and, dysregulation of iron content or distribution can result in intracellular iron accumulation, which can lead to the damage of cells, tissues, and organs. Elaborate regulatory systems have evolved to maintain iron levels at sufficient yet safe concentrations in cells. Such homeostasis of iron metabolism is achieved by the coordination of iron uptake, utilization, recycling, storage, and export [27]. The iron dependency of ferroptosis was initially demonstrated by the use of iron cdheepleantodresntcoy ionfhfiebrirtofpetrorsoipstwosaiss.inAitdiadliltyiodneamlloyn, sintrathteedsbamy tehsetuusdeyo, firioronnrechspeloantosirvsetoelienmhiebnitt bfeirnrdoipntgospirso. Pesetratbulribshatiinogntohfaitrofenrrmopettaobsiosliissminctarincabteeltyrigmgoedreudlaitnedmbuyltiiprolenwmaeytsabsuoclihsmas. dPierretcutrobxaitdioantioonf oirfoinromnebtaybFoIlNismO2c,aanpbeerotrxigidgee-rceodnitnaimniunlgtipcloemwpaoyusnsdu,choraisrdonireucpt toaxkideawtiiothn oufltirraosnmbayllFnINanOo2-, paapretircolexsid[e2-8c,2o9n]t.aSiniminiglarcloym, spaoliunnodm,yocrinir, oann aunpttiabkaectweriitahl durlturga,scmaanllalnsaontoripgagretricfleersro[2p8t,o2s9i]s. bSiymsielqaurleys, tsearliinngomofyicroinn, iannlaynsotisboamcteesri[a3l0d].rAuglt,hcoaungahlstohetreigxagcetrmfeercrohpantoissmissbtyhsreoquugehswtehriincgh pcrpHpofatinuueefrolkecflelrnorilroneuucrctmeyg,ooteel,ianvnsseonrwrsteceincozeihrgeiensersrauoaoddftnolfloegnyiafirsaiessftrrcfis,aimooouruncoosnpansgisornltschikomcfttttmaaaeaisuhoescynitreseetnstnoitrhispfn[aoenre3ertbfgvrio0olcnporuue]acoflor.leenfiapatsensAocctetmrscieiofnrnellersiottsigthriirf(pasaeoeFoofttllrrfineauoeegorcivsgofmfurhtieaohposiraranm.nertrsitotTonh1ipmsttnph)eihaou.setucefnoetfteisaxescni,rpniblraraseorcgoocnaoatrtlpefryepni,emstnmctorcmcotereeshiaosralicairlisplhn(usen.FtaollogaTueianfgnsevhrniiuidasusciimrnrmnlssoeehp,tetanso1hnatarwo)thencs,.hitcoyfitirmeemimnovrlcgluruhipeutogolayofltpea.snhrittprrtHgao/rwliesoseereiihporxsismennitpic,aoseohtwhnschrriodhesetcem,ceahdssoilnmeeoltiguosinowsncprlssmauiatoizmratgsrseissevtiudi/cr,tiseloathoatxyinniesrs--
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