Role of CELF2 in ferroptosis: Potential targets for cancer therapy (Review)

Li, Jason; Lu, Xian; Zhu, Zhihong; Wang, Yan; Zhang, Wenlei; Zheng, Ruipeng; Xue, Wei; Li, Jiarui

doi:10.3892/ijmm.2023.5291

Cited by 2 publications

(3 citation statements)

References 197 publications

(248 reference statements)

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“…CELF2 is a critical tumor suppressor in a variety of tumors that inhibits proliferation and promotes apoptosis of cancer cells (41)(42)(43). Moreover, CELF2 can directly bind mRNAs of ferroptosis regulators (13). In this study, we found that CELF2 expression was elevated in both AKI models, but it was decreased by miR-208a-3p.…”

Section: Discussionmentioning

confidence: 52%

“…Apoptosis is an important form of renal tubular epithelial cell death (40). Ferroptosis is a new regulated cell death program (13). Inhibition of ferroptosis has been found to be a promising therapeutic strategy for the protection of tubular epithelial cells against I/R injury (9).…”

Section: Discussionmentioning

confidence: 99%

“…Ferroptosis is characterized by an excessive accumulation of iron-dependent lipid peroxide resulted from excessive intracellular levels of reactive oxygen species (ROS) (13). Glutathione peroxidase 4 (GPX4), solute carrier family 7 member 11 (SLC7A11), and acyl-CoA synthetase long-chain family member 4 (ACSL4) are vital regulators of ferroptosis (the detailed descriptions of related factors and proteins are shown in supplemental table 1, http://links.…”

Section: Introductionmentioning

confidence: 99%

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miR-208a-3p regulated by circUQCRC2 suppresses ischemia/reperfusion-induced acute kidney injury by inhibiting CELF2-mediated tubular epithelial cell apoptosis, inflammation and ferroptosis

Huang,

Meng,

Pang

et al. 2024

Shock

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Background Acute kidney injury (AKI) is a prevalent clinical syndrome with persistent kidney dysfunction. Renal ischemia/reperfusion (I/R) injury is a major cause of AKI. miR-208a-3p overexpression attenuated myocardial I/R injury. This study aims to investigate the role and mechanism of miR-208a-3p in I/R-induced AKI. Methods AKI models were established using hypoxia/reoxygenation (H/R)-exposed tubule epithelial cell HK-2 and I/R-induced mice. The function and mechanism of miR-208a-3p were investigated by gain-or loss-of-function methods using real-time PCR, CCK-8, flow cytometry, ELISA, western blot, hematoxylin-eosin staining, Tunel assay, detection of Fe2+, ROS, BUN and Creatinine, and luciferase reporter assay. Results miR-208a-3p expression was suppressed, while the expression of CELF2 and circular RNA ubiquinol-cytochrome c reductase core protein 2 (circUQCRC2) was increased in both AKI models. miR-208a-3p upregulation or circUQCRC2 silencing increased the viability, decreased the levels of proinflammatory cytokines (TNF-α, IL-1β and IL-6), reduced apoptosis and contents of Fe2+ and ROS, elevated expression of GPX4 and SLC7A11, reduced ACSL4 expression in H/R-stimulated HK-2 cells. Also, miR-208a-3p improved kidney function by alleviating renal injury, apoptosis, inflammation and ferroptosis in AKI mouse model. CELF2 was a target gene of miR-208a-3p which was negatively modulated by circUQCRC2. Overexpression of CELF2 blocked the function of miR-208a-3p upregulation or circUQCRC2 silencing on H/R-treated HK-2 cells. Moreover, the effects of circUQCRC2 downregulation on H/R-injured cells were also reversed by miR-208a-3p inhibitor. Conclusions miR-208a-3p regulated by circUQCRC2 could attenuate I/R-induced AKI by inhibiting CELF2-mediated tubular epithelial cell apoptosis, inflammation and ferroptosis. This study provides potential therapeutic targets for I/R-induced AKI.

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