TRPML1 contributes to antimony-induced nephrotoxicity by initiating ferroptosis via chaperone-mediated autophagy

Liu, Lei; Luo, Chao; Zheng, Dongnan; Wang, Xuehai; Wang, Rui; Ding, Wenjie; Shen, Zhaoping; Xue, Peng; Yu, Shali; Liu, Yifei; Zhao, Xinyuan

doi:10.1016/j.fct.2023.114378

Cited by 4 publications

(2 citation statements)

References 27 publications

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“…Previous studies have suggested that the divalent metal transporter (DMT1) is an endolysosomal iron transporter responsible for transporting free Fe 2+ to the cytoplasm, and inhibition of DMT1 can enhance the mortality rate of CSCs [ 49 ]. Similar to DMT1, the endolysosomal ion channel TRPML1 also mediates the release of Fe 2+ from lysosome to the cytosol, and its roles in regulating ferroptosis have also been revealed in recent studies [ 50 , 51 ]. In this study, we also found that the TRPML1 inhibitor ML-SI1 could induce ferroptosis in CSCs and decrease their proportion in breast cancer cells.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of lysosomal TRPML1 channel eliminates breast cancer stem cells by triggering ferroptosis

Fan,

Wu,

et al. 2024

Cell Death Discov.

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Cancer stem cells (CSCs) are a sub-population of cells possessing high tumorigenic potential, which contribute to therapeutic resistance, metastasis and recurrence. Eradication of CSCs is widely recognized as a crucial factor in improving patient prognosis, yet the effective targeting of these cells remains a major challenge. Here, we show that the lysosomal cation channel TRPML1 represents a promising target for CSCs. TRPML1 is highly expressed in breast cancer cells and exhibits sensitivity to salinomycin, a drug known to selectively eliminate CSCs. Pharmacological inhibition and genetic depletion of TRPML1 promote ferroptosis in breast CSCs, reduce their stemness, and enhance the sensitivity of breast cancer cells to chemotherapy drug doxorubicin. The inhibition and knockout of TRPML1 also demonstrate significant suppression of tumor formation and growth in the mouse xenograft model. These findings suggest that targeting TRPML1 to eliminate CSCs may be an effective strategy for the treatment of breast cancer.

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Section: Discussionmentioning

confidence: 99%

Inhibition of lysosomal TRPML1 channel eliminates breast cancer stem cells by triggering ferroptosis

Fan,

Wu,

et al. 2024

Cell Death Discov.

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“…The first includes erastin, which reduces GSH levels by inhibiting system Xcand affects voltage-dependent anion channels (VDACs) for mitochondrial dysfunction. Erastin also enhances lysosomalassociated membrane protein 2a, promoting chaperone-mediated autophagy and GPX4 degradation (13)(14)(15)(16). The second category, with members like RSL3 and DPI7, directly inhibits GPX4 (17,18).…”

Section: Introductionmentioning

confidence: 99%

Deciphering the link: ferroptosis and its role in glioma

Wang,

Liu,

Che

et al. 2024

Front. Immunol.

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Glioma, as the most frequently occurring primary malignancy in the central nervous system, significantly impacts patients’ quality of life and cognitive abilities. Ferroptosis, a newly discovered form of cell death, is characterized by significant iron accumulation and lipid peroxidation. This process is fundamentally dependent on iron. Various factors inducing ferroptosis can either directly or indirectly influence glutathione peroxidase, leading to reduced antioxidant capabilities and an increase in lipid reactive oxygen species (ROS) within cells, culminating in oxidative cell death. Recent research indicates a strong connection between ferroptosis and a range of pathophysiological conditions, including tumors, neurological disorders, ischemia-reperfusion injuries, kidney damage, and hematological diseases. The regulation of ferroptosis to intervene in the progression of these diseases has emerged as a major area of interest in etiological research and therapy. However, the exact functional alterations and molecular mechanisms underlying ferroptosis remain to be extensively studied. The review firstly explores the intricate relationship between ferroptosis and glioma, highlighting how ferroptosis contributes to glioma pathogenesis and how glioma cells may resist this form of cell death. Then, we discuss recent studies that have identified potential ferroptosis inducers and inhibitors, which could serve as novel therapeutic strategies for glioma. We also examine the current challenges in targeting ferroptosis in glioma treatment, including the complexity of its regulation and the need for precise delivery methods. This review aims to provide a comprehensive overview of the current state of research on ferroptosis in glioma, offering insights into future therapeutic strategies and the broader implications of this novel cell death pathway in cancer biology.

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Construction of metal interpretable scoring system and identification of tungsten as a novel risk factor in COPD

Wang,

Cheng

et al. 2024

Ecotoxicology and Environmental Safety

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TRPML1 contributes to antimony-induced nephrotoxicity by initiating ferroptosis via chaperone-mediated autophagy

Cited by 4 publications

References 27 publications

Inhibition of lysosomal TRPML1 channel eliminates breast cancer stem cells by triggering ferroptosis

Inhibition of lysosomal TRPML1 channel eliminates breast cancer stem cells by triggering ferroptosis

Deciphering the link: ferroptosis and its role in glioma

Construction of metal interpretable scoring system and identification of tungsten as a novel risk factor in COPD

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