The role of microRNAs in ferroptosis

Guo, Liqing; Zhang, Qingkun; Liu, Yuehui

doi:10.3389/fmolb.2022.1003045

Cited by 10 publications

(8 citation statements)

References 109 publications

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“…In 2012, the concept of ferroptosis was proposed by Stockwell, and is characterized by Fe 2+ dependence, lipid peroxidation, and depletion of REDOX systems. Ferroptosis is involved in various diseases, such as malignant tumors, neurodegeneration, and ischemia–reperfusion injury 57 . As a result, molecules and drugs targeting ferroptosis have become a hot topic of research and development 58 .…”

Section: Discussionmentioning

confidence: 99%

MiR-122-5p regulates erastin-induced ferroptosis via CS in nasopharyngeal carcinoma

Guo,

Wang,

et al. 2024

Sci Rep

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Nasopharyngeal carcinoma (NPC) is a tumor that occurs in the nasopharynx. Although advances in detection and treatment have improved the prognosis of NPC the treatment of advanced NPC remains challenging. Here, we explored the effect of microRNA (miR)-122-5p on erastin-induced ferroptosis in NPC cells and the role of ferroptosis in the development of NPC. The effect of miR-122-5p silencing and overexpression and the effect of citrate synthase on erastin-induced lipid peroxidation in NPC cells was analyzed by measuring the amounts of malondialdehyde, Fe2+, glutathione, and reactive oxygen species and the morphological alterations of mitochondria. The malignant biological behavior of NPC cells was examined by cell counting kit-8, EDU, colony formation, Transwell, and wound healing assays. The effects of miR-122-5p on cell proliferation and migration associated with ferroptosis were examined in vivo in a mouse model of NPC generated by subcutaneous injection of NPC cells. We found that erastin induced ferroptosis in NPC cells. miR-122-5p overexpression inhibited CS, thereby promoting erastin-induced ferroptosis in NPC cells and decreasing NPC cell proliferation, migration, and invasion.

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Section: Discussionmentioning

confidence: 99%

MiR-122-5p regulates erastin-induced ferroptosis via CS in nasopharyngeal carcinoma

Guo,

Wang,

et al. 2024

Sci Rep

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“…Increasing evidence has indicated that ferroptosis is associated with cancer initiation, progression, and suppression [ 45 ]. Furthermore, miRNAs can either promote or suppress tumors through regulating ferroptosis by interfering with iron metabolism, lipid peroxidation, and the system Xc - /GPX4 axis [ 46 , 47 ]. EVO can affect the expression of non-coding RNAs and their target genes in cancer cells, suggesting that EVO can mediate gene expression at the post-transcriptional level.…”

Section: Discussionmentioning

confidence: 99%

Evodiamine Exhibits Anti-Bladder Cancer Activity by Suppression of Glutathione Peroxidase 4 and Induction of Ferroptosis

Shan

et al. 2023

IJMS

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Evodiamine (EVO) exhibits anti-cancer activity through the inhibition of cell proliferation; however, little is known about its underlying mechanism. To determine whether ferroptosis is involved in the therapeutic effects of EVO, we investigated critical factors, such as lipid peroxidation levels and glutathione peroxidase 4 (GPX4) expression, under EVO treatment. Our results showed that EVO inhibited the cell proliferation of poorly differentiated, high-grade bladder cancer TCCSUP cells in a dose- and time-dependent manner. Lipid peroxides were detected by fluorescence microscopy after cancer cell exposure to EVO. GPX4, which catalyzes the conversion of lipid peroxides to prevent cells from undergoing ferroptosis, was decreased dose-dependently by EVO treatment. Given the features of iron dependency and lipid-peroxidation-driven death in ferroptosis, the iron chelator deferoxamine (DFO) was used to suppress EVO-induced ferroptosis. The lipid peroxide level significantly decreased when cells were treated with DFO prior to EVO treatment. DFO also attenuated EVO-induced cell death. Co-treatment with a pan-caspase inhibitor or necroptosis inhibitor with EVO did not alleviate cancer cell death. These results indicate that EVO induces ferroptosis rather than apoptosis or necroptosis. Furthermore, EVO suppressed the migratory ability, decreased the expression of mesenchymal markers, and increased epithelial marker expression, determined by a transwell migration assay and Western blotting. The TCCSUP bladder tumor xenograft tumor model confirmed the effects of EVO on the inhibition of tumor growth and EMT. In conclusion, EVO is a novel inducer for activating the ferroptosis of bladder cancer cells and may be a potential therapeutic agent for bladder cancer.

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Section: Introductionmentioning

confidence: 99%

“…Some studies focused on exploring the role of miRNAs in regulating ferroptosis [ 35 , 36 , 37 ]. Several miRNAs that modulate cardiomyopathy, neuronal injury, and cancer-associated ferroptosis are summarized [ 35 ]. Ferroptosis-regulating miRNAs [ 36 , 37 ] and circular RNAs [ 36 ] occurring in several cancer cells are summarized [ 36 ].…”

Section: Introductionmentioning

confidence: 99%

Ferroptosis-Regulated Natural Products and miRNAs and Their Potential Targeting to Ferroptosis and Exosome Biogenesis

Chuang,

Yen,

Chien

et al. 2024

IJMS

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Ferroptosis, which comprises iron-dependent cell death, is crucial in cancer and non-cancer treatments. Exosomes, the extracellular vesicles, may deliver biomolecules to regulate disease progression. The interplay between ferroptosis and exosomes may modulate cancer development but is rarely investigated in natural product treatments and their modulating miRNAs. This review focuses on the ferroptosis-modulating effects of natural products and miRNAs concerning their participation in ferroptosis and exosome biogenesis (secretion and assembly)-related targets in cancer and non-cancer cells. Natural products and miRNAs with ferroptosis-modulating effects were retrieved and organized. Next, a literature search established the connection of a panel of ferroptosis-modulating genes to these ferroptosis-associated natural products. Moreover, ferroptosis-associated miRNAs were inputted into the miRNA database (miRDB) to bioinformatically search the potential targets for the modulation of ferroptosis and exosome biogenesis. Finally, the literature search provided a connection between ferroptosis-modulating miRNAs and natural products. Consequently, the connections from ferroptosis–miRNA–exosome biogenesis to natural product-based anticancer treatments are well-organized. This review sheds light on the research directions for integrating miRNAs and exosome biogenesis into the ferroptosis-modulating therapeutic effects of natural products on cancer and non-cancer diseases.

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The role of microRNAs in ferroptosis

Cited by 10 publications

References 109 publications

MiR-122-5p regulates erastin-induced ferroptosis via CS in nasopharyngeal carcinoma

MiR-122-5p regulates erastin-induced ferroptosis via CS in nasopharyngeal carcinoma

Evodiamine Exhibits Anti-Bladder Cancer Activity by Suppression of Glutathione Peroxidase 4 and Induction of Ferroptosis

Ferroptosis-Regulated Natural Products and miRNAs and Their Potential Targeting to Ferroptosis and Exosome Biogenesis

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