Ferroptosis: the vulnerability within a cancer monster

Xie, Wei‐Fen; Yu, Jindan

doi:10.1172/jci170027

Cited by 9 publications

(3 citation statements)

References 28 publications

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“…The upstream molecular of ACSL4, cyclin-dependent kinase 1 (CDK1) can mediate ubiquitin-mediated degradation of ACSL4 via phosphorylating ACSL4 and recruiting ubiquitin ligase E3 component N-recognition protein 5 (UBR5), ultimately causing ferroptosis and chemotherapy resistance in CRC [138]. RB1 is another upstream suppressor of ACSL4, whose loss can activate transcription factor E2F1 binding to the promoter of ACSL4 by increasing the transcriptional levels of E2F1, thus promoting the occurrence of ferroptosis [139]. These findings provide a novel therapeutic target for RB1-deficient cancers.…”

Section: Fatty Acidsmentioning

confidence: 99%

Metabolism-regulated ferroptosis in cancer progression and therapy

Ye,

Wen,

Qin

et al. 2024

Cell Death Dis

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Cancer metabolism mainly includes carbohydrate, amino acid and lipid metabolism, each of which can be reprogrammed. These processes interact with each other to adapt to the complicated microenvironment. Ferroptosis is a regulated cell death induced by iron-dependent lipid peroxidation, which is morphologically different from apoptosis, necrosis, necroptosis, pyroptosis, autophagy-dependent cell death and cuprotosis. Cancer metabolism plays opposite roles in ferroptosis. On the one hand, carbohydrate metabolism can produce NADPH to maintain GPX4 and FSP1 function, and amino acid metabolism can provide substrates for synthesizing GPX4; on the other hand, lipid metabolism might synthesize PUFAs to trigger ferroptosis. The mechanisms through which cancer metabolism affects ferroptosis have been investigated extensively for a long time; however, some mechanisms have not yet been elucidated. In this review, we summarize the interaction between cancer metabolism and ferroptosis. Importantly, we were most concerned with how these targets can be utilized in cancer therapy.

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Section: Fatty Acidsmentioning

confidence: 99%

Metabolism-regulated ferroptosis in cancer progression and therapy

Ye,

Wen,

Qin

et al. 2024

Cell Death Dis

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“…This is consistent with the fact that GPX4 is abundantly expressed in most cancer cells. However, this strong ferroptotic potential is unblocked when RB1-deficient cells are treated with GPX4 inhibitors, resulting in massive ferroptosis [98].…”

Section: Pathways Associated With Both Iron Death and Tumor Progressionmentioning

confidence: 99%

Ferroptosis in Cancer Progression

Zhang

Chen

Wang

et al. 2023

Cells

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Ferroptosis is a newly discovered iron-dependent form of regulated cell death driven by phospholipid peroxidation and associated with processes including iron overload, lipid peroxidation, and dysfunction of cellular antioxidant systems. Ferroptosis is found to be closely related to many diseases, including cancer at every stage. Epithelial–mesenchymal transition (EMT) in malignant tumors that originate from epithelia promotes cancer-cell migration, invasion, and metastasis by disrupting cell–cell and cell–cell matrix junctions, cell polarity, etc. Recent studies have shown that ferroptosis appears to share multiple initiators and overlapping pathways with EMT in cancers and identify ferroptosis as a potential predictor of various cancer grades and prognoses. Cancer metastasis involves multiple steps, including local invasion of cancer cells, intravasation, survival in circulation, arrest at a distant organ site, extravasation and adaptation to foreign tissue microenvironments, angiogenesis, and the formation of “premetastatic niche”. Numerous studies have revealed that ferroptosis is closely associated with cancer metastasis. From the cellular perspective, ferroptosis has been implicated in the regulation of cancer metastasis. From the molecular perspective, the signaling pathways activated during the two events interweave. This review briefly introduces the mechanisms of ferroptosis and discusses how ferroptosis is involved in cancer progression, including EMT, cancer angiogenesis, invasion, and metastasis.

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Section: Relationship Between Ferroptosis and Cancer Angiogenesis Inv...mentioning

confidence: 99%

Ferroptosis in Cancer Progression

Zhang¹,

Chen²,

Wang³

et al. 2023

Preprint

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Ferroptosis is a newly discovered iron-dependent form of regulated cell death driven by phospholipid peroxidation, associated with processes including iron overload, lipid peroxidation and dysfunction of cellular antioxidant systems. Ferroptosis is found closely related to many diseases including cancer, at its every stage. Epithelial-mesenchymal transition (EMT) in malignant tumors that originate from epithelia promotes cancer cell migration, invasion and metastasis by disrupting cell-cell and cell-martrix junctions, cell polarity, etc. Recent studies have shown that ferroptosis appears to share multiple initiators and overlapping pathways with EMT in cancers and identify ferroptosis as a potential predictor of various cancer grade and prognosis. Cancer metastasis involves multiple steps including local invasion of cancer cells, intravasation, survival in circulation, arrest at a distant organ site, extravasation and adaptation to foreign tissue microenvironments, angiogenesis and the formation of “premetastatic niche”. Numerous studies have revealed that ferroptosis is closely associated with cancer metastasis. From the cellular perspective, ferroptosis has been implicated in the regulation of cancer metastasis. From the molecular perspective, the signaling pathways activated during the two events interweave. This review briefly introduces the mechanisms of ferroptosis, and discusses how ferroptosis is involved in cancer progression including EMT, cancer angiogenesis, invasion and metastasis.

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Ferroptosis: the vulnerability within a cancer monster

Cited by 9 publications

References 28 publications

Metabolism-regulated ferroptosis in cancer progression and therapy

Metabolism-regulated ferroptosis in cancer progression and therapy

Ferroptosis in Cancer Progression

Ferroptosis in Cancer Progression

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