Interleukin-10 control of pre-miR155 maturation involves CELF2

Yoon, Jeff S. J.; Wu, Mike K.; Zhu, Tian Hao; Zhao, Helen; Cheung, Sylvia T.; Chamberlain, Thomas C.; Mui, Alice

doi:10.1371/journal.pone.0231639

Cited by 6 publications

(18 citation statements)

References 48 publications

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“…CELF2 is reported to be associated with IL10 (Interleukin-10) to inhibit the maturation of pre-miR155 by blocking KSRP (KH-Type Splicing Regulatory Protein). In this way, it can be considered as negative regulator of miR155 [36]. Similar results are reported for miR140, where CELF1/2 binding interferes with DICER binding to miR140 and thus inhibits its maturation [43].…”

Section: General Characteristics Of the Celf Protein Familysupporting

confidence: 73%

“…In the cytoplasm, CELF proteins are involved in mRNA stability, translation, alternative polyadenylation (APA), and pre-miRNA maturation [12,32,[34][35][36]. CELFs regulate mRNA stability across the genome, although only specific, well-studied events are discussed in this section.…”

Section: General Characteristics Of the Celf Protein Familymentioning

confidence: 99%

“…CELF2 was recently discovered to be a possible regulator of pre-miR155 maturation, with CELF2 knockdown reducing IL10's ability to block pre-miR155 processing. CELF2 binding to pre-miR155 may hamper DICER's capacity to bind to and cleave pre-miR155 [36]. Other proteins required for pre-miR155 processing, such as KH-type splicing regulatory protein (KSRP), may also be blocked by CELF2 binding to pre-miR155 [153].…”

Section: Noncoding Rna Regulation By Celfmentioning

confidence: 99%

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CELF Family Proteins in Cancer: Highlights on the RNA-Binding Protein/Noncoding RNA Regulatory Axis

Aghdam

Jave‐Suárez

2021

IJMS

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Post-transcriptional modifications to coding and non-coding RNAs are unquestionably a pivotal way in which human mRNA and protein diversity can influence the different phases of a transcript’s life cycle. CELF (CUGBP Elav-like family) proteins are RBPs (RNA-binding proteins) with pleiotropic capabilities in RNA processing. Their responsibilities extend from alternative splicing and transcript editing in the nucleus to mRNA stability, and translation into the cytoplasm. In this way, CELF family members have been connected to global alterations in cancer proliferation and invasion, leading to their identification as potential tumor suppressors or even oncogenes. Notably, genetic variants, alternative splicing, phosphorylation, acetylation, subcellular distribution, competition with other RBPs, and ultimately lncRNAs, miRNAs, and circRNAs all impact CELF regulation. Discoveries have emerged about the control of CELF functions, particularly via noncoding RNAs, and CELF proteins have been identified as competing, antagonizing, and regulating agents of noncoding RNA biogenesis. On the other hand, CELFs are an intriguing example through which to broaden our understanding of the RBP/noncoding RNA regulatory axis. Balancing these complex pathways in cancer is undeniably pivotal and deserves further research. This review outlines some mechanisms of CELF protein regulation and their functional consequences in cancer physiology.

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Section: General Characteristics Of the Celf Protein Familysupporting

confidence: 73%

Section: General Characteristics Of the Celf Protein Familymentioning

confidence: 99%

Section: Noncoding Rna Regulation By Celfmentioning

confidence: 99%

See 1 more Smart Citation

CELF Family Proteins in Cancer: Highlights on the RNA-Binding Protein/Noncoding RNA Regulatory Axis

Aghdam

Jave‐Suárez

2021

IJMS

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“…Recently, Simmonds et al showed that LPS stimulation leads to the early expression of miR-155-3p, followed by miR-155-5p [26]. Thus, in the current study, we investigated whether CELF2 or another protein called Far Upstream element Binding Protein 1 (FUBP1), which we also observed to bind to pre-miR-155 [25], might be involved in regulating miR-155-3p levels.…”

Section: Introductionmentioning

confidence: 76%

“…We previously showed that IL10 inhibits the maturation of pre-miR-155 into mature miR-155-5p [18]. We then used mass spectrometry to identify proteins that bind to pre-miR-155 to characterize the mechanism by which IL10R signaling inhibits pre-miR-155 maturation [25]. We found CUGBP Elav-Like Family member 2 (CELF2) protein associates with pre-miR-155 in an IL10 dependent manner, and deletion of CELF2 enhanced LPS-induced expression of miR-155-5p suggesting that CELF2's role is to inhibit miR-155-5p expression.…”

Section: Introductionmentioning

confidence: 99%

The Strand Specific Regulation of miR-155-3p in Response to Lipopolysaccharide and Interleukin-10 Stimulation Requires FUBP1 Protein

Yoon¹,

Baksh²,

Chamberlain³

et al. 2021

Preprint

Self Cite

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MicroRNA-155 (miR-155) expression promotes inflammatory responses in macrophages. Activation of macrophages with lipopolysaccharide (LPS) elevates miR-155, while the anti-inflammatory cytokine interleukin-10 (IL10) reduces miR-155 levels. MiR-155 exists in two forms, miR-155-5p and miR-155-3p, produced from the precursor of miR-155 (pre-miR-155). MiR-155-5p is the most abundant strand in activated macrophages, but in response to LPS, the miR-155-3p level is upregulated first, followed by miR-155-5p later. We have previously identified CELF2 protein which interacts with pre-miR-155 and impairs miR-155-5p expression. We now show that CELF2 only regulates the miR-155-5p expression and that another protein FUBP1 controls miR-155-3p levels in response to LPS and IL10.

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MicroRNA-155 expression is associated with pulpitis progression by targeting SHIP1

Guo

et al. 2022

Mol Biol Rep

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Pulpitis is a commonly seen oral in ammation condition in clinical practice, it can cause much pain for the patient and may induce infections in other systems. Much is still unknown for the pathogenic mechanism of pulpitis. In this work, we discovered that the expression of miR-155 was associated with dental pulpal in ammation both in vivo and in vitro. Experiments on odontoblast cell line MDPC-23 showed miR-155 could act as a positive regulator by increasing the production of pro-in ammatory cytokines IL-1β and IL-6 during in ammatory responses, whereas knockdown of miR-155 can reverse the effects. Bioinformatics analysis demonstrated that SHIP1 is a direct target of miR-155 in odontoblasts, this result was further veri ed at both mRNA and protein level. Inhibition of miR-155 resulted in the downregulation of in ammation factors, while co-transfection of si-SHIP1 and miR-155 inhibitor promoted the in ammatory responses. Treatment with miR-155 mimic or si-SHIP1 up-regulated the protein level of p-PI3K and p-AKT. By contrast, miR-155 inhibitor exerted the opposite effects. miR-155 mimics could upregulate the gene expression of IL-1β and IL-6. Co-transfection of LY294002 and miR-155 mimic attenuated the in ammatory responses. Consistent with in vitro results, miR-155 −/− mice could alleviate in ammatory response, as well as decrease the activation of p-PI3K and p-AKT, whereas increase the activation of SHIP1. In conclusion, these data revealed a novel role for miR-155 in regulation of dental pulpal in ammatory response by targeting SHIP1 through PI3K/AKT signaling pathway.

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Interleukin-10 control of pre-miR155 maturation involves CELF2

Cited by 6 publications

References 48 publications

CELF Family Proteins in Cancer: Highlights on the RNA-Binding Protein/Noncoding RNA Regulatory Axis

CELF Family Proteins in Cancer: Highlights on the RNA-Binding Protein/Noncoding RNA Regulatory Axis

The Strand Specific Regulation of miR-155-3p in Response to Lipopolysaccharide and Interleukin-10 Stimulation Requires FUBP1 Protein

MicroRNA-155 expression is associated with pulpitis progression by targeting SHIP1

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