Prolonged exposure to environmental levels of microcystin-LR triggers ferroptosis in brain via the activation of Erk/MAPK signaling pathway

Zhu, Lingyun; Cao, Pingping; Yang, Suisui; Lin, Fan; Wang, Jing

doi:10.1016/j.ecoenv.2023.115651

Cited by 4 publications

(3 citation statements)

References 66 publications

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“…2E ). Additionally, KEGG pathway analysis revealed that the 'MAPK signaling pathway' ( 51 , 52 ), 'Hippo signaling pathway' ( 53 ) and 'Wnt signaling pathway' ( 54 ) were enriched ( Fig. 2F ), suggesting that DElncRNAs are involved in ferroptosis.…”

Section: Resultsmentioning

confidence: 99%

“…S2A-C ), suggesting that ferroptosis inducer-induced upregulation of LUCAT1 may be common in different types of cancer. Furthermore, the top three GO terms for LUCAT1 predicted by the LncACTdb were 'superoxide metabolic process' ( 55 ), 'MAPK activity' ( 51 , 52 ) and 'oxygen and reactive oxygen species metabolic process' ( 56 ), which all have important roles in ferroptosis ( Fig. 2O ).…”

Section: Resultsmentioning

confidence: 99%

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Long non‑coding RNA lung cancer‑associated transcript 1 regulates ferroptosis via microRNA‑34a‑5p‑mediated GTP cyclohydrolase 1 downregulation in lung cancer cells

Tai,

Zhai,

Ding

et al. 2024

Int J Oncol

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Ferroptosis, a recently discovered type of programmed cell death triggered by excessive accumulation of iron-dependent lipid peroxidation, is linked to several malignancies, including non-small cell lung cancer. Long non-coding RNAs (lncRNAs) are involved in ferroptosis; however, data on their role and mechanism in cancer therapy remains limited. Therefore, the aim of the present study was to identify ferroptosis-associated mRNAs and lncRNAs in A549 lung cancer cells treated with RAS-selective lethal 3 (RSL3) and ferrostatin-1 (Fer-1) using RNA sequencing. The results demonstrated that lncRNA lung cancer-associated transcript 1 (LUCAT1) was significantly upregulated in lung adenocarcinoma and lung squamous cell carcinoma tissues. Co-expression analysis of differentially expressed mRNAs and lncRNAs suggested that LUCAT1 has a crucial role in ferroptosis. LUCAT1 expression was markedly elevated in A549 cells treated with RSL3, which was prevented by co-incubation with Fer-1. Functionally, overexpression of LUCAT1 facilitated cell proliferation and reduced the occurrence of ferroptosis induced by RSL3 and Erastin, while inhibition of LUCAT1 expression reduced cell proliferation and increased ferroptosis. Mechanistically, downregulation of LUCAT1 resulted in the downregulation of both GTP cyclohydrolase 1 (GCH1) and ferroptosis suppressor protein 1 (FSP1). Furthermore, inhibition of LUCAT1 expression upregulated microRNA (miR)-34a-5p and then downregulated GCH1. These results indicated that inhibition of LUCAT1 expression promoted ferroptosis by modulating the downregulation of GCH1, mediated by miR-34a-5p. Therefore, the combination of knocking down LUCAT1 expression with ferroptosis inducers may be a promising strategy for lung cancer treatment.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Long non‑coding RNA lung cancer‑associated transcript 1 regulates ferroptosis via microRNA‑34a‑5p‑mediated GTP cyclohydrolase 1 downregulation in lung cancer cells

Tai,

Zhai,

Ding

et al. 2024

Int J Oncol

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show abstract

“…Gpx4 is a member of the GPX protein family responsible for converting cytotoxic lipid peroxides to non‐toxic lipid alcohols by transforming glutathione (GSH) to oxidized glutathione (GSSG), 100 thereby preserving cell membrane integrity. 101 Glutathione reductase (GSR) can convert GSSH back to GSH by FAD (flavin adenine dinucleotide) prosthetic group and NADPH, thus contributing to the maintenance of glutathione (GSH) homeostasis and cellular protection against oxidative damage. 102 , 103 In various in vitro and in vivo conditions, genetic ablation or pharmacological inhibition of Gpx4 can lead to uncontrolled lipid peroxidation and trigger severe ferroptosis.…”

Section: The Molecular Mechanism Of Ferroptosismentioning

confidence: 99%

Mechanism of ferroptosis regulating ischemic stroke and pharmacologically inhibiting ferroptosis in treatment of ischemic stroke

Chai,

Zheng,

Shen

2024

CNS Neurosci Ther

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Ferroptosis is a newly discovered form of programmed cell death that is non‐caspase‐dependent and is characterized by the production of lethal levels of iron‐dependent lipid reactive oxygen species (ROS). In recent years, ferroptosis has attracted great interest in the field of cerebral infarction because it differs morphologically, physiologically, and genetically from other forms of cell death such as necrosis, apoptosis, autophagy, and pyroptosis. In addition, ROS is considered to be an important prognostic factor for ischemic stroke, making it a promising target for stroke treatment. This paper summarizes the induction and defense mechanisms associated with ferroptosis, and explores potential treatment strategies for ischemic stroke in order to lay the groundwork for the development of new neuroprotective drugs.

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Ferroptosis implication in environmental-induced neurotoxicity

Zhang,

Xie

2024

Science of The Total Environment

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Prolonged exposure to environmental levels of microcystin-LR triggers ferroptosis in brain via the activation of Erk/MAPK signaling pathway

Cited by 4 publications

References 66 publications

Long non‑coding RNA lung cancer‑associated transcript 1 regulates ferroptosis via microRNA‑34a‑5p‑mediated GTP cyclohydrolase 1 downregulation in lung cancer cells

Long non‑coding RNA lung cancer‑associated transcript 1 regulates ferroptosis via microRNA‑34a‑5p‑mediated GTP cyclohydrolase 1 downregulation in lung cancer cells

Mechanism of ferroptosis regulating ischemic stroke and pharmacologically inhibiting ferroptosis in treatment of ischemic stroke

Ferroptosis implication in environmental-induced neurotoxicity

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