Ilf3 and <scp>NF90</scp> functions in <scp>RNA</scp> biology

Castella, Sandrine; Bernard, Rozenn; Corno, Mélanie; Fradin, Aurélie; Larcher, Jean-Christophe

doi:10.1002/wrna.1270

Cited by 110 publications

(115 citation statements)

References 90 publications

(223 reference statements)

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“…Nuclear factor 90 (NF90), a major spliced form of interleukin enhancer binding factor 3 (ILF3), was first identified on the basis of its ability to bind to the IL2 promoter in activated T cells [23], and it was subsequently found to bind double-stranded (ds) RNA structural elements [24]. Recent studies have shown that NF90 forms a complex with NF45 and plays multifunctional roles in the cells, including transcription, and microRNA biogenesis [25].…”

Section: Introductionmentioning

confidence: 99%

LincIN, a novel NF90-binding long non-coding RNA, is overexpressed in advanced breast tumors and involved in metastasis

et al. 2017

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BackgroundRecent genome-wide profiling by sequencing and distinctive chromatin signatures has identified thousands of long non-coding RNA (lncRNA) species (>200 nt). LncRNAs have emerged as important regulators of gene expression, involving in both developmental and pathological processes. While altered expression of lncRNAs has been observed in breast cancer development, their roles in breast cancer progression and metastasis are still poorly understood.MethodsTo identify novel breast cancer-associated lncRNA candidates, we employed a high-density SNP array-based approach to uncover intergenic lncRNA genes that are aberrantly expressed in breast cancer. We first evaluated the potential value as a breast cancer prognostic biomarker for one breast cancer-associated lncRNA, LincIN, using a breast cancer cohort retrieved from The Cancer Genome Atlas (TCGA) Data Portal. Then we characterized the role of LincIN in breast cancer progression and metastasis by in vitro invasion assay and a mouse tail vein injection metastasis model. To study the action of LincIN, we identified LincIN-interacting protein partner(s) by RNA pull-down experiments followed with protein identification by mass spectrometry.ResultsHigh levels of LincIN expression are frequently observed in tumors compared to adjacent normal tissues, and are strongly associated with aggressive breast cancer. Importantly, analysis of TCGA data further suggest that high expression of LincIN is associated with poor overall survival in patients with breast cancer (P = 0.044 and P = 0.011 after adjustment for age). The functional experiments demonstrate that knockdown of LincIN inhibits tumor cell migration and invasion in vitro, which is supported by the results of transcriptome analysis in the LincIN-knockdown cells. Furthermore, knockdown of LincIN diminishes lung metastasis in a mouse tail vein injection model. We also identified a LincIN-binding protein, NF90, through which overexpression of LincIN may repress p21 protein expression by inhibiting its translation, and upregulation of p21 by LincIN knockdown may be associated with less aggressive metastasis phenotypes.ConclusionsOur studies provide clear evidence to support LincIN as a new regulator of tumor progression-metastasis at both transcriptional and translational levels and as a promising prognostic biomarker for breast cancer.Electronic supplementary materialThe online version of this article (doi:10.1186/s13058-017-0853-2) contains supplementary material, which is available to authorized users.

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Section: Introductionmentioning

confidence: 99%

LincIN, a novel NF90-binding long non-coding RNA, is overexpressed in advanced breast tumors and involved in metastasis

et al. 2017

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“…1B). [22][23][24] Analyses of these candidate targets in CF cells indicated that CSNK1G2 and IF3/NF90 mRNA levels were comparable in CF and control cells. However, RPTOR mRNA was significantly lower in IB3-1CF cells than in IB3-1/S9 control cells and thus subsequent analyses focused on the role RPTOR in regulating the CF disease phenotype.…”

Section: Identification Of Candidate Targets Of Mir-155 In Cfmentioning

confidence: 99%

RPTOR, a novel target of miR-155, elicits a fibrotic phenotype of cystic fibrosis lung epithelium by upregulating CTGF

et al. 2016

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(2016) RPTOR, a novel target of miR-155, elicits a fibrotic phenotype of cystic fibrosis lung epithelium by upregulating CTGF, RNA Biology, 13:9, 837-847, DOI: 10.1080/15476286.2016 ABSTRACTCystic fibrosis (CF) is an autosomal recessive disorder caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene, the most frequent of which is F508del-CFTR. CF is characterized by excessive secretion of pro-inflammatory mediators into the airway lumen, inducing a highly inflammatory cellular phenotype. This process triggers fibrosis, causing airway destruction and leading to high morbidity and mortality. We previously reported that miR-155 is upregulated in CF lung epithelial cells, but the molecular mechanisms by which miR-155 affects the disease phenotype is not understood. Here we report that RPTOR (regulatory associated protein of mTOR, complex 1) is a novel target of miR-155 in CF lung epithelial cells. The suppression of RPTOR expression and subsequent activation of TGF-b signaling resulted in the induction of fibrosis by elevating connective tissue growth factor (CTGF) abundance in CF lung epithelial cells. Thus, we propose that miR-155 might regulate fibrosis of CF lungs through the increased CTGF expression, highlighting its potential value in CF therapy.

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“…Using unbiased mass spectrometry to identify mRNA stability factors modified by IL-19, we identified an RBP termed ILF3 (interleukin enhancer binding factor 3) (16). In humans, ILF3 is also known as NF90, NFAR1, and DRBP76 (17). They are all transcribed from the ILF3 gene; although they are used interchangeably, most often they are referred to as ILF3, the gene they are transcribed from.…”

mentioning

confidence: 99%

“…They are all transcribed from the ILF3 gene; although they are used interchangeably, most often they are referred to as ILF3, the gene they are transcribed from. ILF3 is primarily known for its role in innate immunity by participation in cellular antiviral responses (17). ILF3 has been shown to regulate transcription (18)(19)(20), post-transcriptional RNA stabilization (21)(22)(23), nuclear export (17), and translation in response to viral infection (19,21).…”

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confidence: 99%

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RNA stability protein ILF3 mediates cytokine‐induced angiogenesis

et al. 2018

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Interleukin enhancer‐binding factor 3 (ILF3), an RNA‐binding protein, is best known for its role in innate immunity by participation in cellular antiviral responses. A role for ILF3 in angiogenesis is unreported. ILF3 expression in CD31+ capillaries of hypoxic cardiac tissue was detected by immunohistochemistry. Proangiogenic stimuli induce ILF3 mRNA and protein expression in cultured human coronary artery endothelial cells (hCAECs). Angiogenic indices, including proliferation, migration, and tube formation, are all significantly reduced in hCAECs when ILF3 is knocked down using small interfering RNA (siRNA), but are significantly increased when ILF3 is overexpressed using adenovirus. Protein and mRNA abundance of several angiogenic factors including CXCL1, VEGF, and IL‐8 are decreased when ILF3 is knocked down by siRNA. These factors are increased when ILF3 is overexpressed by adenovirus. ILF3 is phosphorylated and translocates from the nucleus to the cytoplasm in response to angiogenic stimuli. Proangiogenic transcripts containing adenine and uridine‐rich elements were bound to ILF3 through RNA immunoprecipitation. ILF3 stabilizes proangiogenic transcripts including VEGF, CXCL1, and IL‐8 in hCAECs. Together these data suggest that in endothelial cells, the RNA stability protein, ILF3, plays a novel and central role in angiogenesis. Our working hypothesis is that ILF3 promotes angiogenesis through cytokine‐inducible mRNA stabilization of proangiogenic transcripts.—Vrakas, C. N., Herman, A. B., Ray, M., Kelemen, S. E., Scalia, R., Autieri, M. V. RNA stability protein ILF3 mediates cytokine‐induced angiogenesis. FASEB J. 33, 3304–3316 (2019). http://www.fasebj.org

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Ilf3 and NF90 functions in RNA biology

Cited by 110 publications

References 90 publications

LincIN, a novel NF90-binding long non-coding RNA, is overexpressed in advanced breast tumors and involved in metastasis

LincIN, a novel NF90-binding long non-coding RNA, is overexpressed in advanced breast tumors and involved in metastasis

RPTOR, a novel target of miR-155, elicits a fibrotic phenotype of cystic fibrosis lung epithelium by upregulating CTGF

RNA stability protein ILF3 mediates cytokine‐induced angiogenesis

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