ArticleExperimental and therapeutic medicine2021
IGF2BP2 knockdown inhibits LPS-induced pyroptosis in BEAS-2B cells by targeting caspase 4, a crucial molecule of the non-canonical pyroptosis pathway.
Article in Experimental and therapeutic medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- IGF2BP2 Regulates the Progression of Alzheimer's Disease Through m6A-Mediated NLRP3 Inflammasome.Immunity, inflammation and disease · 2025Article
- Causal effects of gut microbiota on sepsis and sepsis-related death: insights from genome-wide Mendelian randomization, single-cell RNA, bulk RNA sequencing, and network pharmacology.Journal of translational medicine · 2024Article
- IGF2BP2‑dependent STIM1 inhibition protects against LPS‑induced pneumoniaExperimental and therapeutic medicine · 2023Article
- Role of PIM2 in acute lung injury induced by sepsis.Experimental and therapeutic medicine · 2022Article
- Article
- The landscape of circular RNA in preterm birth.Frontiers in immunology · 2022Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Insulin-like growth factor 2 (IGF2) mRNA-binding protein 2 (IGF2BP2) is a secreted protein that can bind to IGF2 and has been reported to promote inflammation. The data from the ENCORI database have predicted that IGF2BP2 can bind caspase 4, which mediates pyroptosis and promotes airway inflammation and lipopolysaccharide (LPS)-induced lung injury. The present study investigated whether IGF2BP2 can regulate LPS-induced lung cell inflammation by targeting caspase 4. Therefore, the non-tumorigenic lung epithelial cell line Beas-2B was transfected with short hairpin RNA (shRNA)-IGF2BP2 and stimulated with LPS. A number of parameters, including cell viability, production of interleukin (IL)-1β and IL-18, activation of gasdermin D (GSDMD) and the expression levels of IGF2BP2, caspase 4 and cleaved-caspase 1, were subsequently assessed using CCK-8, ELISA kits, western blotting and immunofluorescence staining, respectively. RNA pull-down assay was used to probe the possible interaction between IGF2BP2 and caspase 4 RNA. LPS treatment was found to inhibit cell viability, trigger IL-1β and IL-18 production and increase IGF2BP2 expression in a concentration-dependent manner. Compared with cells transfected with shRNA-negative control, cells that were transfected with shRNA-IGF2BP2 exhibited enhanced cell viability, reduced IL-1β and IL-18 concentrations, decreased GSDMD activation in addition to reduced expression levels of caspase 4 and cleaved-caspase 1 following stimulation with 1 µg/ml LPS. Concomitantly, the effects of IGF2BP2 silencing on caspase 4 expression were higher compared with those noted on caspase 1. In addition, binding of IGF2BP2 to caspase 4 RNA was also observed. To conclude, data from the present study suggest that IGF2BP2 knockdown inhibited LPS-induced Beas-2B cell inflammation by targeting caspase 4, thereby inhibiting the non-canonical pyroptosis pathway.
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