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The role of ferroptosis in lung cancer.

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TLDR
In this article, the authors summarized the core mechanism and regulatory network of ferroptosis in lung cancer cells, and highlighted the induction-related tumor therapies, which may provide new insights for targeted lung cancer therapy.
Abstract
Lung cancer is one of the most common cancers in the world. Although medical treatment has made impressive progress in recent years, it is still one of the leading causes of cancer-related deaths in men and women. Ferroptosis is a type of non-apoptotic cell death modality, usually characterized by iron-dependent lipid peroxidation, rather than caspase-induced protein cleavage. Excessive or lack of ferroptosis is associated with a variety of diseases, including cancer and ischaemia-reperfusion injury. Recent preclinical evidence suggests that targeting ferroptotic pathway is a potential strategy for the treatment of lung cancer. In this review, we summarize the core mechanism and regulatory network of ferroptosis in lung cancer cells, and highlight ferroptosis induction-related tumor therapies. The reviewed information may provide new insights for targeted lung cancer therapy.

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Journal ArticleDOI

The Selenoprotein Glutathione Peroxidase 4: From Molecular Mechanisms to Novel Therapeutic Opportunities

TL;DR: This current report aims to review the literature underlying all insights and present an up-to-date perspective on the current understanding of GPX4 as a potential therapeutic target.
Journal ArticleDOI

Evidence of pyroptosis and ferroptosis extensively involved in autoimmune diseases at the single-cell transcriptome level

TL;DR: In this paper , the aberrant trend of ferroptosis and pyproptosis-related genes were analyzed in several representative autoimmune diseases (psoriasis, atopic dermatitis, vitiligo, multiple sclerosis, systemic sclerosis-associated interstitial lung disease, Crohn's disease, and experimental autoimmune orchitis).
Journal ArticleDOI

Ferroptosis and Its Role in Chronic Diseases

TL;DR: The basic characteristics of ferroptosis, its regulation, as well as the relationship between ferroPTosis and chronic diseases such as cancer, nervous system diseases, metabolic diseases, and inflammatory bowel diseases are summarized.
Journal ArticleDOI

Evidence of pyroptosis and ferroptosis extensively involved in autoimmune diseases at the single-cell transcriptome level

TL;DR: In this article , the aberrant trend of ferroptosis and pyproptosis-related genes were analyzed in several representative autoimmune diseases (psoriasis, atopic dermatitis, vitiligo, multiple sclerosis, systemic sclerosis-associated interstitial lung disease, Crohn's disease, and experimental autoimmune orchitis).
Journal ArticleDOI

CircP4HB regulates ferroptosis via SLC7A11-mediated glutathione synthesis in lung adenocarcinoma

TL;DR: The role of circRNAs in lung adenocarcinoma (LUAD) ferroptosis remains unclear as mentioned in this paper , however, the role of CircRNAs play a key role in the development of different types of cancer.
References
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Journal ArticleDOI

Ferroptosis: An Iron-Dependent Form of Nonapoptotic Cell Death

TL;DR: This paper identified the small molecule ferrostatin-1 as a potent inhibitor of ferroptosis in cancer cells and glutamate-induced cell death in organotypic rat brain slices, suggesting similarities between these two processes.
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Regulation of Ferroptotic Cancer Cell Death by GPX4

TL;DR: Targeted metabolomic profiling and chemoproteomics revealed that GPX4 is an essential regulator of ferroptotic cancer cell death and sensitivity profiling in 177 cancer cell lines revealed that diffuse large B cell lymphomas and renal cell carcinomas are particularly susceptible to GPx4-regulated ferroPTosis.
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Ferroptosis as a p53-mediated activity during tumour suppression

TL;DR: It is shown that p53 inhibits cystine uptake and sensitizes cells to ferroptosis, a non-apoptotic form of cell death, by repressing expression of SLC7A11, a key component of the Cystine/glutamate antiporter.
Journal ArticleDOI

ACSL4 dictates ferroptosis sensitivity by shaping cellular lipid composition

TL;DR: Pharmacological targeting of ACSL4 with thiazolidinediones, a class of antidiabetic compound, ameliorated tissue demise in a mouse model of ferroptosis, suggesting that ACSL 4 inhibition is a viable therapeutic approach to preventing ferroPTosis-related diseases.
Journal ArticleDOI

The CoQ oxidoreductase FSP1 acts parallel to GPX4 to inhibit ferroptosis.

TL;DR: AFerroptosis suppressor protein 1 (FSP1) is identified as a key component of a non-mitochondrial CoQ antioxidant system that acts in parallel to the canonical glutathione-based GPX4 pathway, and pharmacological inhibition of FSP1 may provide an effective strategy to sensitize cancer cells to ferroPTosis-inducing chemotherapeutic agents.
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