N6-Methyladenosine-modified circSAV1 triggers ferroptosis in COPD through recruiting YTHDF1 to facilitate the translation of IREB2

Xia, Haibo; Wu, Yan; Zhao, Jing; Cheng, Cheng; Lin, Jiaheng; Yang, Yi; Lu, Lu; Xiang, Qiaojun; Bian, Tao; Liu, Qizhan

doi:10.1038/s41418-023-01138-9

Cited by 52 publications

(21 citation statements)

References 47 publications

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“…S4 ). IGF2BP3 can recruit RNA stabilizers ( 27 ), YTHDF1 can facilitate mRNA translation efficiency ( 28 ), and YTHDC1 can recruit the RNA splicing and control the nuclear export ( 29 ). These biological functions are inconsistent with their expression levels and the reduced expression level of RRAS.…”

Section: Resultsmentioning

confidence: 99%

METTL3/YTHDF2 m6A axis promotes the malignant progression of bladder cancer by epigenetically suppressing RRAS

Chen

Wang

et al. 2023

Oncol Rep

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The present study aimed to explore the potential roles of the methyltransferase-like 3 (METTL3)-mediated methylation of RAS related (RRAS) mRNA in the tumorigenesis and development of bladder cancer (BCa). For this purpose, the relative expression levels of METTL3 in BCa specimens and cell lines were measured using reverse transcription-quantitative PCR (RT-qPCR) and western blot analysis. The association between the METTL3 expression level and the clinical characteristics of patients with BCa was analyzed using The Cancer Genome Atlas (TCGA) and Gene Expression Profiling Interactive Analysis databases. Cellular experiments were performed to confirm the effects of METTL3 on the proliferative, migratory and invasive capacities of BCa cells. RT-qPCR, western blot analysis, methylated RNA immunoprecipitation (MeRIP)-qPCR and dual-luciferase report assays were utilized to verify the METTL3/RRAS/YTH N 6 -methyladenosine (m6A) RNA binding protein 2 (YTHDF2) regulatory axis in BCa. The results revealed that METTL3 expression was markedly increased in BCa specimens and cell lines, and was associated with poor clinical characteristics of patients with BCa. In vitro and in vivo assays demonstrated that the silencing of METTL3 markedly suppressed the proliferative, migratory and invasive capacities of BCa cells. MeRIP-PCR and dual-luciferase report assays indicated that METTL3 could bind to the m6A sites of RRAS mRNA and suppress the transcriptional activity of RRAS. YTHDF2 could recognize the m6A sites of RRAS and mediate RRAS degradation. On the whole, the findings of the present study reveal the pivotal role of METTL3-catalyzed m6A modification in BCa tumorigenesis and development. The change could facilitate BCa tumor growth and metastasis by suppressing RRAS expression in an m6A YTHDF2-dependent manner. Targeting the METTL3/RRAS/YTHDF2 regulatory axis may thus prove to be a promising strategy for the diagnosis and therapy of BCa.

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Section: Resultsmentioning

confidence: 99%

METTL3/YTHDF2 m6A axis promotes the malignant progression of bladder cancer by epigenetically suppressing RRAS

Chen

Wang

et al. 2023

Oncol Rep

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“…27 protein 1 (YTHDF1), and thus circSAV1-dependent ferroptosis represents a therapeutic target for COPD. 28 Together, the results of the aforementioned studies demonstrate that specific circRNAs possess the ability to influence ferroptosis in lung cancer cells. Accordingly, if circRNA expression can be manipulated to increase ferroptosis among tumor cells, such approaches could potentially contribute to the treatment of lung cancer.…”

Section: Disease Of the Respiratory Systemmentioning

confidence: 87%

“…Xia et al. found that N6‐methyladenosine‐modified circSAV1 can trigger ferroptosis in chronic obstructive pulmonary disease (COPD) by promoting iron‐responsive element‐binding protein 2 (IREB2) translation through recruitment of YTH N6‐methyladenosine RNA binding protein 1 (YTHDF1), and thus circSAV1‐dependent ferroptosis represents a therapeutic target for COPD 28 . Together, the results of the aforementioned studies demonstrate that specific circRNAs possess the ability to influence ferroptosis in lung cancer cells.…”

Section: Circrnas Regulate Ferroptosis In Diseasementioning

confidence: 99%

CircRNA and ferroptosis in human disease: Insights for new treatments

Liu,

Zhou,

Cao

2023

Anim Models and Exp Med

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Circular RNA (circRNA), classified as a type of non‐coding RNA, has gained significant attention in the field of biology due to its distinctive ring structure and functional properties. Recent research has provided evidence that specific circRNAs have the ability to modulate disease progression through diverse mechanisms, one of which is by regulating cellular ferroptosis. Ferroptosis is a form of regulated cell death that is driven by iron dependency and lipid peroxidation, and extensive investigations have revealed a relationship between ferroptosis and disease development. In addition to evidence that both circRNAs and ferroptosis exert critical roles in disease progression, circRNAs have also been shown to actively mediate the process of ferroptosis. The relationship between circRNAs and ferroptosis therefore influences disease progression and offers novel targets for disease treatment. By directly or indirectly modulating the expression of circRNAs that regulate the expression of ferroptosis‐related proteins, it may be possible to impact disease progression by promoting or inhibiting ferroptosis. Current research indicates such approaches may hold significant value in a wide variety of common diseases across physiological systems. This review comprehensively summarizes the findings of recent studies investigating the roles of circRNAs in the regulation of ferroptosis in various diseases.

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“…Normally, the human body relies on ferroptosis to remove damaged or pathological cells. However, dysregulation of ferroptosis can promote the development of multiple human diseases (Y. Jiang, Qiao, et al, 2023; Sarparast et al, 2023; H. Xia et al, 2023). Researchers have shown increasing enthusiasm for the role of ferroptosis in cancer development.…”

Section: Conclusion and Future Perspectivementioning

confidence: 99%

Ferroptosis: Potential opportunities for natural products in cancer therapy

Nie,

Shen,

Zhou

et al. 2023

Phytotherapy Research

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Cancer cells often exhibit defects in the execution of cell death, resulting in poor clinical outcomes for patients with many cancer types. Ferroptosis is a newly discovered form of programmed cell death characterized by intracellular iron overload and lipid peroxidation in the cell membrane. Increasing evidence suggests that ferroptosis is closely associated with a wide variety of physiological and pathological processes, particularly in cancer. Notably, various bioactive natural products have been shown to induce the initiation and execution of ferroptosis in cancer cells, thereby exerting anticancer effects. In this review, we summarize the core regulatory mechanisms of ferroptosis and the multifaceted roles of ferroptosis in cancer. Importantly, we focus on natural products that regulate ferroptosis in cancer cells, such as terpenoids, polyphenols, alkaloids, steroids, quinones, and polysaccharides. The clinical efficacy, adverse effects, and drug–drug interactions of these natural products need to be evaluated in further high‐quality studies to accelerate their application in cancer treatment.

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N6-Methyladenosine-modified circSAV1 triggers ferroptosis in COPD through recruiting YTHDF1 to facilitate the translation of IREB2

Cited by 52 publications

References 47 publications

METTL3/YTHDF2 m6A axis promotes the malignant progression of bladder cancer by epigenetically suppressing RRAS

METTL3/YTHDF2 m6A axis promotes the malignant progression of bladder cancer by epigenetically suppressing RRAS

CircRNA and ferroptosis in human disease: Insights for new treatments

Ferroptosis: Potential opportunities for natural products in cancer therapy

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