Inhibition of miR-1224 suppresses hypoxia/reoxygenation-induced oxidative stress and apoptosis in cardiomyocytes through targeting GPX4

Li, Guibin; Jin, Jiali; Liu, Shengxin; Ding, Kejun; Qian, Caizhen

doi:10.1016/j.yexmp.2021.104645

Cited by 12 publications

(5 citation statements)

References 28 publications

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“…Previous studies have revealed that the translation of GPX4 mRNA is under the regulation of various RNA binding proteins, such as guanine-rich sequence-binding factor 1, deleted in azoospermia-associated protein 1 and SECIS binding protein 2 (28)(29)(30). Moreover, GPX4 mRNA was also revealed to be directly subjected to the regulation of miRNAs such as miR-214-3p, miR-1224, miR-324-3p and miR-541-3p (31)(32)(33)(34). These findings revealed the complexity of the post-transcriptional regulation of GPX4.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of SND1 overcomes chemoresistance in bladder cancer cells by promoting ferroptosis

et al. 2022

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Chemotherapy remains one of the most important adjuvant treatments for bladder cancer (BC). However, similar to other malignancies, BC is prone to chemotherapy resistance and only approximately half of muscle-invasive patients with BC respond to chemotherapy. The present study aimed to reveal the mechanisms underlying chemoresistance in BC cells. Cell viabilities were assessed by CCK-8 assay. The differentiated expression of genes in chemoresistant and their parental BC cells were examined by RNA sequencing. Cell death was determined by flow cytometry. Different cell death inhibitors were used to determine the types of cell death. Levels of reactive oxygen species, iron, glutathione and malondialdehyde were assessed using the corresponding commercial kits. ChIP and dual luciferase activity assays were performed to investigate the interaction between staphylococcal nuclease and tumour domain containing 1 (SND1) and glutathione peroxidase 4 (GPX4) mRNA. RNAi was used to knockdown SND1 or GPX4. The results revealed that SND1 in BC cells were insensitive to cisplatin, and inhibition of SND1 overcame this resistance. Silencing of SND1 enhanced cell death induced by cisplatin by promoting ferroptosis in BC cells. Mechanistically, SND1 was revealed to bind to the 3'UTR region of GPX4 mRNA and stabilise it. Knockdown of GPX4 could also overcome chemoresistance, and overexpressing GPX4 reversed the effects of silencing of GPX4 on the chemosensitivity of BC cells. Thus, targeting the SND1-GPX4 axis may be a potential strategy to overcome chemoresistance in BC cells.

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Section: Discussionmentioning

confidence: 99%

Inhibition of SND1 overcomes chemoresistance in bladder cancer cells by promoting ferroptosis

et al. 2022

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“…Cells in the logarithmic growth phase were incubated in 6-well plates for 24 h for stabilization; then, the medium was replaced with DMEM with or without 0.5–50 μ g/mL ABLP for 12 h and then incubated with 50 μ M H 2 O 2 for 0.5 h. After treatment, the cells were washed with fresh DMEM three times and then incubated with 10 μ M DCFH-DA at 37°C for 30 min. Ultimately, the fluorescence intensity of cells was observed under a fluorescence microscope, and data were evaluated using Image J software (National Institutes of Health, Bethesda, MD, USA) [ 9 , 10 ].…”

Section: Methodsmentioning

confidence: 99%

Anshen Buxin Liuwei Pill, a Mongolian Medicinal Formula, Could Protect H2O2-Induced H9c2 Myocardial Cell Injury by Suppressing Apoptosis, Calcium Channel Activation, and Oxidative Stress

Dong

Tong

Huang

et al. 2022

Evidence-Based Complementary and Alternative Medicine

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Background. Anshen Buxin Liuwei pill (ABLP) is a Mongolian medicinal formula which has a therapeutic effect on the symptoms such as coronary heart disease, angina pectoris, arrhythmia, depression and irritability, palpitation, and short breath. However, its bioactivity against cardiac injury remains unclear. Methods. The protective effect of ABLP was evaluated using H9c2 cells. Cell viability, intracellular Ca2+, reactive oxidative indices, and mitochondrial membrane potential (∆ψ) were assessed, respectively. The mRNA levels of Ca2+ channel-related genes (DHPR, RyR2, and SCN5A) and oxidative stress-related genes (Keap1, Nrf2, and HO-1) were measured by RT-PCR. Results. 0.5–50 μg/mL ABLP could significantly decrease H2O2-induced cell injury by suppressing cell necrosis/apoptosis and excess oxidative stress, ameliorating the collapse of ∆ψ, and reducing intracellular Ca2+ concentration. Furthermore, 0.5–50 μg/mL ABLP reversed H2O2-induced imbalance in the mRNA levels of DHPR, RyR2, SCN5A, Keap1, Nrf2, and HO-1 gene in H9c2 cells, which further illustrate the mechanism. Conclusion. ABLP provided protective and therapeutic benefits against H2O2-induced H9c2 cell injury, indicating that this formula can effectively treat coronary disease. In addition, the present study also provides an in-depth understanding of the pharmacological functions of ABLP, which may lead to further successful applications of Mongolian medicine.

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“…Therefore, lncRNA LINC00618 represses SLC7A11 expression to accelerate ferroptosis in human leukemia [266]. Similarly, GPX4 was reported to be targeted to induce ferroptosis by miR-541-3p and miR-214-3p in liver cancer [143,267], miR-324-3p in breast cancer [144] and kidney cancer [145], miR-1231 in thyroid cancer [268], miR-1287-5p/miR-744-5p/miR-615-3p in lung cancer [269,270], miR-1287-5p in osteosarcoma [271], miR-15a in prostate cancer [272], miR-193a-5p in cervical cancer [273], miR-3202 in cholangiocarcinoma [274], as well as by miR-182-5p, miR-1224, miR-15a-5p, miR-135b-3p in the IRI of kidney injury [254] and heart [275][276][277], miR-23a-3p in intracerebral hemorrhage [278], miR-188 in diabetic nephropa- Similarly, GPX4 was reported to be targeted to induce ferroptosis by miR-541-3p and miR-214-3p in liver cancer [143,267], miR-324-3p in breast cancer [144] and kidney cancer [145], miR-1231 in thyroid cancer [268], miR-1287-5p/miR-744-5p/miR-615-3p in lung cancer [269,270], miR-1287-5p in osteosarcoma [271], miR-15a in prostate cancer [272], miR-193a-5p in cervical cancer [273], miR-3202 in cholangiocarcinoma [274], as well as by miR-182-5p, miR-1224, miR-15a-5p, miR-135b-3p in the IRI of kidney injury [254] and heart [275][276][277], miR-23a-3p in intracerebral hemorrhage [278], miR-188 in diabetic nephropathy [279], miR-761 in liver dysfunction of patients with polycystic ovary syndrome [198], exosomal miR-208a/b secre...…”

Section: Ncrnas Regulating Ferroptosis Through Antioxidant Defensementioning

confidence: 99%

The Regulation of Ferroptosis by Noncoding RNAs

Zheng,

Zhang

2023

IJMS

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As a novel form of regulated cell death, ferroptosis is characterized by intracellular iron and lipid peroxide accumulation, which is different from other regulated cell death forms morphologically, biochemically, and immunologically. Ferroptosis is regulated by iron metabolism, lipid metabolism, and antioxidant defense systems as well as various transcription factors and related signal pathways. Emerging evidence has highlighted that ferroptosis is associated with many physiological and pathological processes, including cancer, neurodegeneration diseases, cardiovascular diseases, and ischemia/reperfusion injury. Noncoding RNAs are a group of functional RNA molecules that are not translated into proteins, which can regulate gene expression in various manners. An increasing number of studies have shown that noncoding RNAs, especially miRNAs, lncRNAs, and circRNAs, can interfere with the progression of ferroptosis by modulating ferroptosis-related genes or proteins directly or indirectly. In this review, we summarize the basic mechanisms and regulations of ferroptosis and focus on the recent studies on the mechanism for different types of ncRNAs to regulate ferroptosis in different physiological and pathological conditions, which will deepen our understanding of ferroptosis regulation by noncoding RNAs and provide new insights into employing noncoding RNAs in ferroptosis-associated therapeutic strategies.

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Inhibition of miR-1224 suppresses hypoxia/reoxygenation-induced oxidative stress and apoptosis in cardiomyocytes through targeting GPX4

Cited by 12 publications

References 28 publications

Inhibition of SND1 overcomes chemoresistance in bladder cancer cells by promoting ferroptosis

Inhibition of SND1 overcomes chemoresistance in bladder cancer cells by promoting ferroptosis

Anshen Buxin Liuwei Pill, a Mongolian Medicinal Formula, Could Protect H2O2-Induced H9c2 Myocardial Cell Injury by Suppressing Apoptosis, Calcium Channel Activation, and Oxidative Stress

The Regulation of Ferroptosis by Noncoding RNAs

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