The nuclear factor interleukin 3-regulated (NFIL3) transcription factor involved in innate immunity by activating NF-κB pathway in mud crab Scylla paramamosain

Gu, Wen Bin; Liu, Ze Peng; Zhou, Yi; Li, Bo; Wang, Lan Zhi; Wang, Dong; Chen, Yu Yin; Miao, Shuying

doi:10.1016/j.dci.2019.103452

Cited by 14 publications

(7 citation statements)

References 36 publications

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“…Meanwhile, NFIL3 was recently indicated to exacerbate lung cancer cell migration and invasion of lung cancer cells in a PrPc-dependent manner ( 23 ), while another study demonstrated that NFIL3 exerts function on chromatin to alter cancer cell behavior in the regulation of FOXO-triggered gene expression in cancer ( 24 ). From an inflammation perspective, NFIL3 is known to serve as an important transcription factor of the immune system, wherein NFIL3 silencing can down-regulate the pro-inflammatory cytokine IL-16 ( 25 ). On the other hand, NFIL3 is capable of up-regulating Tim-3 and IL-10 expression as well as T-cell dysfunction ( 26 ).…”

Section: Discussionmentioning

confidence: 99%

RETRACTED: NFIL3 Facilitates Neutrophil Autophagy, Neutrophil Extracellular Trap Formation and Inflammation During Gout via REDD1-Dependent mTOR Inactivation

et al. 2021

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Autophagy pathways play an important role in immunity and inflammation via pathogen clearance mechanisms mediated by immune cells, such as macrophages and neutrophils. In particular, autophagic activity is essential for the release of neutrophil extracellular traps (NETs), a distinct form of active neutrophil death. The current study set out to elucidate the mechanism of the NFIL3/REDD1/mTOR axis in neutrophil autophagy and NET formation during gout inflammation. Firstly, NFIL3 expression patterns were determined in the peripheral blood neutrophils of gout patients and monosodium urate (MSU)-treated neutrophils. Interactions between NFIL3 and REDD1 were identified. In addition, gain- or loss-of-function approaches were used to manipulate NFIL3 and REDD1 in both MSU-induced neutrophils and mice. The mechanism of NFIL3 in inflammation during gout was evaluated both in vivo and in vitro via measurement of cell autophagy, NET formation, MPO activity as well as levels of inflammatory factors. NFIL3 was highly-expressed in both peripheral blood neutrophils from gout patients and MSU-treated neutrophils. NFIL3 promoted the transcription of REDD1 by binding to its promoter. REDD1 augmented neutrophil autophagy and NET formation by inhibiting the mTOR pathway. In vivo experimental results further confirmed that silencing of NFIL3 reduced the inflammatory injury of acute gouty arthritis mice by inhibiting the neutrophil autophagy and NET formation, which was associated with down-regulation of REDD1 and activation of the mTOR pathway. Taken together, NFIL3 can aggravate the inflammatory reaction of gout by stimulating neutrophil autophagy and NET formation via REDD1/mTOR, highlighting NFIL3 as a potential therapeutic target for gout.

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Section: Discussionmentioning

confidence: 99%

RETRACTED: NFIL3 Facilitates Neutrophil Autophagy, Neutrophil Extracellular Trap Formation and Inflammation During Gout via REDD1-Dependent mTOR Inactivation

et al. 2021

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“…Previous research has underscored the pivotal roles played by NFIL3 as regulators of both inflammatory responses 15 , 16 and circadian clock mechanisms 17 . The intricate interplay between immune cells and tumor cells has been long acknowledged 18 .…”

Section: Resultsmentioning

confidence: 99%

A pan-cancer characterization of immune-related NFIL3 identifies potential predictive biomarker

Fei,

Zhang,

Wang

et al. 2024

J. Cancer

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Background: Nuclear factor interleukin 3 (NFIL3) mainly focuses on the regulation of the circadian rhythm and immune system. However, the potential role of NFIL3 in human cancers has not been studied extensively. Methods: We retrieved original data from the TCGA, TARGET, and GTEx datasets via the UCSC Xena browser ( http://genome.ucsc.edu/ ) and integrated them using R version 3.6.4. NFIL3 expression was assessed using resources such as UCSC, GEPIA ( http://gepia.cancer-pku.cn/ ), Kaplan-Meier Plotter (KM Plotter; https://kmplot.com/ ), and the Human Protein Atlas (HPA; https://www.proteinatlas.org/ ) databases. To investigate the prognostic implications of NFIL3, we utilized GEPIA, Kaplan-Meier Plotter, and PrognoScan ( http://www.abren.net/PrognoScan/ ) datasets. For a comprehensive analysis across multiple cancer types, we employed pan-cancer data from UCSC, examining associations between NFIL3 expression and genomic heterogeneity, tumor mutational burden (TMB), microsatellite instability (MSI), tumor purity, and neoantigens. Furthermore, we explored the relationships between NFIL3 expression and the infiltration of immune cells and the expression of immune checkpoint genes. In the context of ovarian cancer, we validated the expression and functional relevance of NFIL3. Cell Counting Kit 8 (CCK8) assays were conducted to assess cell proliferation, while scratch and transwell assays were employed to evaluate cell migration capabilities. We further examined the interaction between NFIL3 and the p53 signaling pathway through quantitative real-time polymerase chain reaction (qRT-PCR), Western blot analysis, immunofluorescence confocal, and Coimmunoprecipitation (Co-IP) assays. Results: In general, NFIL3 expression in cancerous tissues exhibited diminished levels when compared to normal tissue samples. Notably, NFIL3 expression demonstrated a robust correlation with several pivotal aspects, including prognosis, immune cell infiltration, immune checkpoint-related genes, TMB, MSI, tumor purity, and the presence of neoantigens. Experimental investigations involving scratch assays, transwell assays, and assessments of cell proliferation in ovarian cancer cells have provided indications that NFIL3 may exert influence over cell migration and proliferation processes. Moreover, a substantial association between NFIL3 and the p53 signaling pathway was discerned through Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis, with subsequent validation through qRT-PCR, Western blot analysis, immunofluorescence confocal, and co-immunoprecipitation (Co-IP) assays. Conclusions: Therefore, we concluded NFIL3 may serve as a possible prognostic and immunological pan-cancer biomarker.

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“…The hepatopancreas is an important immune organ in crustaceans and plays an important role in regulating the metabolic processes and immune responses of living organisms. Based on our transcriptome data, the DEGs in the hepatopancreas were mainly related to immune and metabolic pathways, whereas DEGs in the muscle were mainly associated with metabolic pathways 3,[24][25][26] .…”

Section: Discussionmentioning

confidence: 99%

“…The expression levels of most of the genes within these pathways were decreased. The hepatopancreas is an important immune organ in crustaceans, it plays an important role in regulating the metabolic processes and immune responses of living organisms 3,[24][25][26] . Among the KEGG enrichment results (Fig.…”

Section: Go and Kegg Enrichment Analysis Of Degsmentioning

confidence: 99%

Transcriptomic analysis of Procambarus clarkii affected by “Black May” disease

Shen

Zhang

Gong

et al. 2020

Sci Rep

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Each year from April to May, high mortality rates are reported in red swamp crayfish (Procambarus clarkii) cultured in Jiangsu and other regions, in China, and this phenomenon has come to be known as “Black May” disease (BMD). Therefore, in order to investigate the possible causes of this disease, this study gathered BMD-affected P. clarkii samples and performed transcriptome analysis on hepatopancreas, gill, and muscle tissues. A total of 19,995,164, 149,212,804, and 222,053,848 clean reads were respectively obtained from the gills, muscle, and hepatopancreas of BMD-affected P. clarkii, and 114,024 unigenes were identified. The number of differentially expressed genes (DEGs) in gill, muscle, and hepatopancreas was 1703, 964, and 476, respectively. GO and KEGG enrichment analyses of the DEGs were then conducted. Based on KEGG pathway enrichment analysis, the most significantly differentially expressed pathways were mainly those involved with metabolism, human disease, and cellular processes. Further analysis of the significantly DEGs revealed that they were mainly related to the mitochondrial-mediated apoptosis pathway and that the expression of these DEGs was mostly down-regulated. Moreover, the expression of genes related to immune and metabolism-related pathways was also significantly down-regulated, and these significantly-inhibited pathways were the likely causes of P. clarkii death. Therefore, our results provide a basis for the identification of BMD causes.

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The nuclear factor interleukin 3-regulated (NFIL3) transcription factor involved in innate immunity by activating NF-κB pathway in mud crab Scylla paramamosain

Cited by 14 publications

References 36 publications

RETRACTED: NFIL3 Facilitates Neutrophil Autophagy, Neutrophil Extracellular Trap Formation and Inflammation During Gout via REDD1-Dependent mTOR Inactivation

RETRACTED: NFIL3 Facilitates Neutrophil Autophagy, Neutrophil Extracellular Trap Formation and Inflammation During Gout via REDD1-Dependent mTOR Inactivation

A pan-cancer characterization of immune-related NFIL3 identifies potential predictive biomarker

Transcriptomic analysis of Procambarus clarkii affected by “Black May” disease

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