Correction: MicroRNA-17-92, a Direct Ap-2α Transcriptional Target, Modulates T-Box Factor Activity in Orofacial Clefting

Wang, J; Bai, Yang; Li, H; Greene, S. L.; Klysik, Elzbieta; Wang, Yu; Rj, Schwartz; Td, Williams; Martin, JF

doi:10.1371/annotation/90602bc3-5052-49ac-a7fb-33210d7c8b4d

Cited by 14 publications

(5 citation statements)

References 28 publications

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“…For example, Ling Li found that the negative feedback loop between E2F1 and miR-17-92 may contribute to palatal development by regulating the proliferation and cell cycle of palatal mesenchymal cells (Li et al, 2017). It has been reported that mutation of miR-17-92 often leads to a severe craniofacial phenotype by targeting the Bmp/AP-2α-miR-17-92-Tbx pathway (Wang et al, 2013). Our previous study found that the miR-146a rs2910164 G allele was associated with the expression of miR-146a, which contributed to the occurrence of oral cleft by regulating TRAF6 expression (Pan et al, 2018).…”

Section: Introductionmentioning

confidence: 94%

Identification of New miRNA-mRNA Networks in the Development of Non-syndromic Cleft Lip With or Without Cleft Palate

Lou

Zhu

et al. 2021

Front. Cell Dev. Biol.

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Objective: To identify new microRNA (miRNA)-mRNA networks in non-syndromic cleft lip with or without cleft palate (NSCL/P).Materials and Methods: Overlapping differentially expressed miRNAs (DEMs) were selected from cleft palate patients (GSE47939) and murine embryonic orofacial tissues (GSE20880). Next, the target genes of DEMs were predicted by Targetscan, miRDB, and FUNRICH, and further filtered through differentially expressed genes (DEGs) from NSCL/P patients and controls (GSE42589), MGI, MalaCards, and DECIPHER databases. The results were then confirmed by in vitro experiments. NSCL/P lip tissues were obtained to explore the expression of miRNAs and their target genes.Results: Let-7c-5p and miR-193a-3p were identified as DEMs, and their overexpression inhibited cell proliferation and promoted cell apoptosis. PIGA and TGFB2 were confirmed as targets of let-7c-5p and miR-193a-3p, respectively, and were involved in craniofacial development in mice. Negative correlation between miRNA and mRNA expression was detected in the NSCL/P lip tissues. They were also associated with the occurrence of NSCL/P based on the MGI, MalaCards, and DECIPHER databases.Conclusions: Let-7c-5p-PIGA and miR-193a-3p-TGFB2 networks may be involved in the development of NSCL/P.

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Section: Introductionmentioning

confidence: 94%

Identification of New miRNA-mRNA Networks in the Development of Non-syndromic Cleft Lip With or Without Cleft Palate

Lou

Zhu

et al. 2021

Front. Cell Dev. Biol.

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“…These findings suggest that the TBX1–miR-200b/200a/429 and miR-203–ZEB2 loop is important for epithelial cell differentiation, EMT, and stemness in the palatal epithelium, and their dysregulation results in CL/P. Indeed, miR-17-92 null mice ( miR-17-92 -/- , miR-17-9 -/- ;miR-106b-25 +/- , and miR-17-92 -/- ;miR-106 -/- mice) display CLP through upregulation of Tbx1 , Tbx3, Fgf10, Shox2, and Osr1 expression [ 101 ]. On the other hand, overexpression of the miR-17-92 cluster suppresses expression of E2F1 , a transcription factor, and inhibits cell proliferation through dysregulation of the cell cycle in mouse embryonic palatal mesenchymal (MEPM) cells [ 102 ].…”

Section: Micrornas Related To Cleft Palatementioning

confidence: 99%

MicroRNAs and Gene Regulatory Networks Related to Cleft Lip and Palate

Iwaya

Suzuki

Iwata

2023

IJMS

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Cleft lip and palate is one of the most common congenital birth defects and has a complex etiology. Either genetic or environmental factors, or both, are involved at various degrees, and the type and severity of clefts vary. One of the longstanding questions is how environmental factors lead to craniofacial developmental anomalies. Recent studies highlight non-coding RNAs as potential epigenetic regulators in cleft lip and palate. In this review, we will discuss microRNAs, a type of small non-coding RNAs that can simultaneously regulate expression of many downstream target genes, as a causative mechanism of cleft lip and palate in humans and mice.

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“…The expression of this gene is upregulated in cutaneous basal cell carcinoma, inversely to miR-451a [ 49 ]. miR-17-92 fine-tunes the expression of Tbx1 in craniofacial development, suggesting miR-17-92 as a candidate genetic modifier for Tbx1 [ 50 ]. Thus, miRNAs both inside and outside the 22q11.2 locus may influence the severity of the clinical phenotypes of DGS/VCFS.…”

Section: Genetics Of Dgs/vcfsmentioning

confidence: 99%

Craniofacial Phenotypes and Genetics of DiGeorge Syndrome

Funato

2022

JDB

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The 22q11.2 deletion is one of the most common genetic microdeletions, affecting approximately 1 in 4000 live births in humans. A 1.5 to 2.5 Mb hemizygous deletion of chromosome 22q11.2 causes DiGeorge syndrome (DGS) and velocardiofacial syndrome (VCFS). DGS/VCFS are associated with prevalent cardiac malformations, thymic and parathyroid hypoplasia, and craniofacial defects. Patients with DGS/VCFS manifest craniofacial anomalies involving the cranium, cranial base, jaws, pharyngeal muscles, ear-nose-throat, palate, teeth, and cervical spine. Most craniofacial phenotypes of DGS/VCFS are caused by proximal 1.5 Mb microdeletions, resulting in a hemizygosity of coding genes, microRNAs, and long noncoding RNAs. TBX1, located on chromosome 22q11.21, encodes a T-box transcription factor and is a candidate gene for DGS/VCFS. TBX1 regulates the fate of progenitor cells in the cranial and pharyngeal apparatus during embryogenesis. Tbx1-null mice exhibit the most clinical features of DGS/VCFS, including craniofacial phenotypes. Despite the frequency of DGS/VCFS, there has been a limited review of the craniofacial phenotypes of DGC/VCFS. This review focuses on these phenotypes and summarizes the current understanding of the genetic factors that impact DGS/VCFS-related phenotypes. We also review DGS/VCFS mouse models that have been designed to better understand the pathogenic processes of DGS/VCFS.

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Correction: MicroRNA-17-92, a Direct Ap-2α Transcriptional Target, Modulates T-Box Factor Activity in Orofacial Clefting

Cited by 14 publications

References 28 publications

Identification of New miRNA-mRNA Networks in the Development of Non-syndromic Cleft Lip With or Without Cleft Palate

Identification of New miRNA-mRNA Networks in the Development of Non-syndromic Cleft Lip With or Without Cleft Palate

MicroRNAs and Gene Regulatory Networks Related to Cleft Lip and Palate

Craniofacial Phenotypes and Genetics of DiGeorge Syndrome

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