Targeting lipid metabolism for ferroptotic cancer therapy

Luo, Min; Yan, Jiajing; Hu, Xinyu; Li, Haolong; Li, Hongsheng; Liu, Quentin; Chen, Yibing; Zou, Zhengzhi

doi:10.1007/s10495-022-01795-0

Cited by 23 publications

(10 citation statements)

References 238 publications

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“…Secondly, as a member of GSTs, GSTP1 could participate in the metabolism of lipids and DNA products derived from oxidative stress. The core of ferroptosis is the excessive accumulation of intracellular lipid peroxides, which is caused by the imbalance of lipid metabolism from various causes (Luo et al, 2022). Besides, Zhao et al find that GSTP1 is a key protein for ferroptosis.…”

Section: Discussionmentioning

confidence: 99%

Targeting GSTP1-dependent ferroptosis in lung cancer radiotherapy: Existing evidence and future directions

Tan

Huang

Niu

et al. 2022

Front. Mol. Biosci.

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Radiotherapy is applied in about 70% patients with tumors, yet radioresistance of tumor cells remains a challenge that limits the efficacy of radiotherapy. Ferroptosis, an iron-dependent lipid peroxidation regulated cell death, is involved in the development of a variety of tumors. Interestingly, there is evidence that ferroptosis inducers in tumor treatment can significantly improve radiotherapy sensitivity. In addition, related studies show that Glutathione S-transferase P1 (GSTP1) is closely related to the development of ferroptosis. The potential mechanism of targeting GSTP1 to inhibit tumor cells from evading ferroptosis leading to radioresistance has been proposed in this review, which implies that GSTP1 may play a key role in radiosensitization of lung cancer via ferroptosis pathway.

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Section: Discussionmentioning

confidence: 99%

Targeting GSTP1-dependent ferroptosis in lung cancer radiotherapy: Existing evidence and future directions

Tan

Huang

Niu

et al. 2022

Front. Mol. Biosci.

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“…The sn1 position can be occupied by either SFA or MUFA, while the sn2 position can be occupied by SFA, MUFA or PUFA [ 8 ]. FA content in PLs is regulated by a variety of mechanisms, including FA synthesis, storage, release and β-oxidation, as well as PL synthesis and PL remodelling [ 9 ]. The content of FAs in PL is regulated through various mechanisms, including FA synthesis, storage, release, β-oxidation, as well as PL synthesis and PL reconstruction [ 9 ].…”

Section: Fatty Acids (Fas)mentioning

confidence: 99%

Ferroptosis and its role in gastric and colorectal cancers

Hou,

Wang,

et al. 2024

Korean J Physiol Pharmacol

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Ferroptosis is a novel mechanism of programmed cell death, characterized by intracellular iron overload, intensified lipid peroxidation, and abnormal accumulation of reactive oxygen species, which ultimately resulting in cell membrane impairment and demise. Research has revealed that cancer cells exhibit a greater demand for iron compared to normal cells, indicating a potential susceptibility of cancer cells to ferroptosis. Stomach and colorectal cancers are common gastrointestinal malignancies, and their elevated occurrence and mortality rates render them a global health concern. Despite significant advancements in medical treatments, certain unfavorable consequences and drug resistance persist. Consequently, directing attention towards the phenomenon of ferroptosis in gastric and colorectal cancers holds promise for enhancing therapeutic efficacy. This review aims to elucidate the intricate cellular metabolism associated with ferroptosis, encompassing lipid and amino acid metabolism, as well as iron metabolic processes. Furthermore, the significance of ferroptosis in the context of gastric and colorectal cancer is thoroughly examined and discussed.

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“…24 Therefore, a decrease in the activity of GPX4 will increase the sensitivity of cells to ferroptosis. 25 Also, the activity of GPX4 closely depends on glutathione (GSH) 26 synthesized from cysteine and glutamate, which has intracellular concentrations and is fine-tuned by the amino acid antiporter system Xc-. 27 Under oxidative conditions, ROS regulate GPX4 expression in two ways: one in which the continuous accumulation of ROS decreases the level of GSH and the expression of GPX4, 28 and the other in which ROS activate p53 and indirectly affect the activity of GPX4.…”

Section: Gpx4-centred Molecular Pathwaymentioning

confidence: 99%

“…GPX4 prevents the toxicity of lipid peroxides and maintains the equilibrium of the membrane lipid bilayer 24 . Therefore, a decrease in the activity of GPX4 will increase the sensitivity of cells to ferroptosis 25 . Also, the activity of GPX4 closely depends on glutathione (GSH) 26 synthesized from cysteine and glutamate, which has intracellular concentrations and is fine‐tuned by the amino acid antiporter system Xc‐ 27 .…”

Section: Ferroptosismentioning

confidence: 99%

Role of oxidative stress‐induced ferroptosis in cancer therapy

Li,

Fan,

Chen

et al. 2024

J Cellular Molecular Medi

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Ferroptosis is a distinct mode of cell death, distinguishing itself from typical apoptosis by its reliance on the accumulation of iron ions and lipid peroxides. Cells manifest an imbalance between oxidative stress and antioxidant equilibrium during certain pathological contexts, such as tumours, resulting in oxidative stress. Notably, recent investigations propose that heightened intracellular reactive oxygen species (ROS) due to oxidative stress can heighten cellular susceptibility to ferroptosis inducers or expedite the onset of ferroptosis. Consequently, comprehending role of ROS in the initiation of ferroptosis has significance in elucidating disorders related to oxidative stress. Moreover, an exhaustive exploration into the mechanism and control of ferroptosis might offer novel targets for addressing specific tumour types. Within this context, our review delves into recent fundamental pathways and the molecular foundation of ferroptosis. Four classical ferroptotic molecular pathways are well characterized, namely, glutathione peroxidase 4‐centred molecular pathway, nuclear factor erythroid 2‐related factor 2 molecular pathway, mitochondrial molecular pathway, and mTOR‐dependent autophagy pathway. Furthermore, we seek to elucidate the regulatory contributions enacted by ROS. Additionally, we provide an overview of targeted medications targeting four molecular pathways implicated in ferroptosis and their potential clinical applications. Here, we review the role of ROS and oxidative stress in ferroptosis, and we discuss opportunities to use ferroptosis as a new strategy for cancer therapy and point out the current challenges persisting within the domain of ROS‐regulated anticancer drug research and development.

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Targeting lipid metabolism for ferroptotic cancer therapy

Cited by 23 publications

References 238 publications

Targeting GSTP1-dependent ferroptosis in lung cancer radiotherapy: Existing evidence and future directions

Targeting GSTP1-dependent ferroptosis in lung cancer radiotherapy: Existing evidence and future directions

Ferroptosis and its role in gastric and colorectal cancers

Role of oxidative stress‐induced ferroptosis in cancer therapy

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