The Molecular Mechanisms of Regulating Oxidative Stress-Induced Ferroptosis and Therapeutic Strategy in Tumors

Zhu, Jinghan; Xiong, Yixiao; Zhang, Yuxin; Wen, Jingyuan; Cai, Ning; Kun, Cheng; Liang, Hang; Zhang, Wanguang

doi:10.1155/2020/8810785

Cited by 82 publications

(63 citation statements)

References 118 publications

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“…Ferroptosis, a necrosis-like type of programmed cell deaths ( 159 ), is attracting attention as a key mechanism involved in the development of future cancer therapies ( 160 , 161 , 162 , 163 ). In ferroptotic cells, the accumulation of lipid peroxides and lipid hydroxyl radicals generated by iron leads to cell death ( 159 , 164 ).…”

Section: New Challenges For Understanding Bach1 At Crossroads Of Cancer Biologymentioning

confidence: 99%

The transcription factor BACH1 at the crossroads of cancer biology: From epithelial–mesenchymal transition to ferroptosis

Igarashi

Nishizawa

Saiki

et al. 2021

Journal of Biological Chemistry

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The progression of cancer involves not only the gradual evolution of cells by mutations in DNA but also alterations in the gene expression induced by those mutations and input from the surrounding microenvironment. Such alterations contribute to cancer cells' abilities to reprogram metabolic pathways and undergo epithelial-to-mesenchymal transition (EMT), which facilitate the survival of cancer cells and their metastasis to other organs. Recently, BTB and CNC homology 1 (BACH1), a heme-regulated transcription factor that represses genes involved in iron and heme metabolism in normal cells, was shown to shape the metabolism and metastatic potential of cancer cells. The growing list of BACH1 target genes in cancer cells reveals that BACH1 promotes metastasis by regulating various sets of genes beyond iron metabolism. BACH1 represses the expression of genes that mediate cell–cell adhesion and oxidative phosphorylation but activates the expression of genes required for glycolysis, cell motility, and matrix protein degradation. Furthermore, BACH1 represses FOXA1 gene encoding an activator of epithelial genes and activates SNAI2 encoding a repressor of epithelial genes, forming a feedforward loop of EMT. By synthesizing these observations, we propose a “two-faced BACH1 model”, which accounts for the dynamic switching between metastasis and stress resistance along with cancer progression. We discuss here the possibility that BACH1-mediated promotion of cancer also brings increased sensitivity to iron-dependent cell death (ferroptosis) through crosstalk of BACH1 target genes, imposing programmed vulnerability upon cancer cells. We also discuss the future directions of this field, including the dynamics and plasticity of EMT.

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Section: New Challenges For Understanding Bach1 At Crossroads Of Cancer Biologymentioning

confidence: 99%

The transcription factor BACH1 at the crossroads of cancer biology: From epithelial–mesenchymal transition to ferroptosis

Igarashi

Nishizawa

Saiki

et al. 2021

Journal of Biological Chemistry

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“…Further studies have shown that FSP1 reduces coenzyme Q10 via NADPH to inhibit ferroptosis ( Zhu et al, 2020 ). The NADPH/FSP1/CoQ10 system is therefore a negative regulator of ferroptosis.…”

Section: Signaling Pathways Of Ferroptosis Associated With Atherosclerosismentioning

confidence: 99%

Ferroptosis Signaling and Regulators in Atherosclerosis

Zhao

Yang

et al. 2021

Front. Cell Dev. Biol.

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Atherosclerosis (AS) is a major cause of cardiovascular diseases such as coronary heart disease, heart failure and stroke. Abnormal lipid metabolism, oxidative stress and inflammation are the main features of AS. Ferroptosis is an iron-driven programmed cell death characterized by lipid peroxidation, which have been proved to participate in the development and progression of AS by different signal pathways. NRF2-Keap1 pathway decreases ferroptosis associated with AS by maintaining cellular iron homeostasis, increasing the production glutathione, GPX4 and NADPH. The p53 plays different roles in ferroptosis at different stages of AS in a transcription-dependent and transcription- independent manner. The Hippo pathway is involved in progression of AS, which has been proved the activation of ferroptosis. Other transcription factors, such as ATF3, ATF4, STAT3, also involved in the occurrence of ferroptosis and AS. Certain proteins or enzymes also have a regulatory role in AS and ferroptosis. In this paper, we review the mechanism of ferroptosis and its important role in AS in an attempt to find a new relationship between ferroptosis and AS and provide new ideas for the future treatment of AS.

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“…Abnormally elevated levels of oxidative stress (ROS) are widely accepted as one of the hallmarks of cancer [ 72 ]. ROS is usually regarded as a toxic substance in cells, and when high ROS cannot be metabolized properly, cells will die or become cancerous.…”

Section: The Association Between Ho-1 and Abnormal Oxidative Stress In Cancer Diseasesmentioning

confidence: 99%

The non-canonical effects of heme oxygenase-1, a classical fighter against oxidative stress

et al. 2021

Redox Biology

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The role of heme oxygenase-1 in resisting oxidative stress and cell protection has always been a hot research topic. With the continuous deepening of research, in addition to directly regulating redox by catalyzing the degradation of heme, HO-1 protein also participates in the gene expression level in a great diversity of methods, thereby initiating cell defense. Particularly the non-canonical nuclear-localized HO-1 and HO-1 protein interactions play the role of a warrior against oxidative stress. Besides, HO-1 may be a promising marker for disease prediction and detection in many clinical trials. Especially for malignant diseases, there may be new advances in the treatment of HO-1 by regulating abnormal ROS and metabolic signaling. The purpose of this review is to systematically sort out and describe several aspects of research to facilitate further detailed mechanism research and clinical application promotion in the future.

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The Molecular Mechanisms of Regulating Oxidative Stress-Induced Ferroptosis and Therapeutic Strategy in Tumors

Cited by 82 publications

References 118 publications

The transcription factor BACH1 at the crossroads of cancer biology: From epithelial–mesenchymal transition to ferroptosis

The transcription factor BACH1 at the crossroads of cancer biology: From epithelial–mesenchymal transition to ferroptosis

Ferroptosis Signaling and Regulators in Atherosclerosis

The non-canonical effects of heme oxygenase-1, a classical fighter against oxidative stress

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