miR-194-5p serves a suppressive role in human keloid fibroblasts via targeting NR2F2

Xu, Qijun; Jiang, Shuhui

doi:10.3892/mmr.2020.11695

Cited by 12 publications

(11 citation statements)

References 35 publications

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“…It has been reported that miR-194 regulates various diseases by targeting genes, such as GRB2-associated binding protein 1 (GAB1) [ 40 ], nuclear receptor subfamily 2 group F member 2 (NR2F2) [ 41 ], NLRP3 [ 42 ], and SLC40A1 [ 43 ]. miRNA regulates post-transcription involved in PCOS-related molecular expression [ 44 , 45 ].…”

Section: Discussionmentioning

confidence: 99%

microRNA-194 is increased in polycystic ovary syndrome granulosa cell and induce KGN cells apoptosis by direct targeting heparin-binding EGF-like growth factor

Lin

et al. 2021

Reprod Biol Endocrinol

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Background Polycystic ovary syndrome (PCOS) is an endocrine-related follicular developmental disorder that affects 50 %-70 % of reproductive-aged women diagnosed with ovulation-related infertility. Abnormal proliferation and apoptosis of granulosa cells (GCs) are thought to be the critical factors leading to abnormal maturation of follicles. It has been shown that microRNAs (miRNAs) exert a significant influence in the pathogenesis of PCOS; however, the relationship between miRNA, PCOS, and GC apoptosis is not entirely understood. Methods To clarify the effect of miR-194 in PCOS, CCK-8, Ki67 staining, AO/EB, and flow cytometry assays were used to assess cell growth, proliferation, and apoptosis in KGN cells, which were artificially stimulated to overexpress miR-194. Luciferase reporter assays and rescue experiments were used to elucidate the mechanism underlying miR-194 in PCOS. Results miR-194 expression was significantly up-regulated in rat models of PCOS and the ovarian GCs of PCOS patients. miR-194 suppression promoted KGN cell growth and proliferation. miR-194 overexpression also induced cell apoptosis, while miR-194 downregulation had an opposite effect. Furthermore, up-regulating heparin-binding EGF-like growth factor (HB-EGF) expression rescued the pro-apoptotic effects of miR-194 upregulation on KGN cells. Conclusions miR-194 is increased in PCOS granulosa cell and may function as a novel biomarker and therapeutic target for KGN cells via HB-EGF regulation.

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Section: Discussionmentioning

confidence: 99%

microRNA-194 is increased in polycystic ovary syndrome granulosa cell and induce KGN cells apoptosis by direct targeting heparin-binding EGF-like growth factor

Lin

et al. 2021

Reprod Biol Endocrinol

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“…Differential miRNA expression profiles have been further identified in fibroblasts derived from keloid and normal skin tissues. 25,86,87 Li and colleagues conducted miRNA microarray analysis on keloid fibroblasts, normal foetal and normal adult skin, and demonstrated that miRNA profiles in keloid fibroblasts were different from adult fibroblasts but similar to foetal fibroblasts, suggesting a transition state to naïve cells in keloid fibroblasts (Pt. info Table S1, row 26).…”

Section: Mirnas In Keloidsmentioning

confidence: 99%

“…86 Finally, nuclear receptor subfamily 2, group F, member 2 (NR2F2) expression was negatively correlated with miRNA-194-5p expression, and the interactome between miRNA-194-5p and NR2F2 appears to be involved in the progression of keloid aggression. 86 Patient concordance for these two studies was excellent in ethnicity (both Han Chinese patients), body site (earlobe, abdomen and back). One study only stated mean patient age rather than age range, and the other study consisted of 90% male patients, so these could not be compared as easily.…”

Section: Mirna-194mentioning

confidence: 99%

“…Aberrant epigenetic patterns have also been found in cell migration and invasion pathways, including histone acetylation, 63,65 miRNAs 76,79,86,96,[103][104][105][110][111][112][113][114] and lncRNAs, 120,121,130,131,136,138 leading to the pathological spread of keloid scars into the surrounding normal tissue.…”

Section: K Eloid Patholog I C Al Pathways Impac Ted By Epi G Ene Ti C Chang Ementioning

confidence: 99%

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The epigenetics of keloids

Stevenson

Deng

Allahham

et al. 2021

Experimental Dermatology

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Keloid scarring is a fibroproliferative disorder of the skin of unknown pathophysiology, characterised by fibrotic tissue that extends beyond the boundaries of the original wound. 1 Keloids develop as a result of disturbance to skin architecture by any wound, and have a strong genetic component, appearing in ethnicities with darker skin pigmentation. 1 There are estimated to be over 11 million keloids in the developed world, with the global number unknown but expected to be higher. 2 Current dogma suggests keloid development follows a similar pathway to normal wound healing but with chronic progression, suggesting disturbance in the fine control of cellular functions that occur during wound healing. 3 Epigenetics, defined as non-base-pair sequence alterations to the DNA, is a key regulator of cell functions, and aberrant epigenetic modifications have been found to contribute to many pathologies, including keloid scars. Our knowledge of progressive fibrosis remains limited, and therapeutic options are few and commonly ineffective, with keloids commonly recurring even after surgery and adjunct treatments. There is an urgent need to gain critical knowledge that will allow us to design better therapeutic strategies and provide evidence to support clinical decisions. This review will explore the current knowledge of the contribution of epigenetic modifications such as DNA methylation, histone modification, microRNAs, long non-coding RNAs to keloid scar formation and progression, and potential treatments utilising modifiers of these processes.

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“…Xu et al found that the expression of miR-194-5p was significantly decreased in KEL FIB cells, and the malignant phenotypes of KEL FIB cells were abated by exogenous upregulation of miR-194-5p. 12 Therefore, the differential expression of miRNAs might play the opposite role in biological function of KFs and keloid.…”

Section: Introductionmentioning

confidence: 99%

Inhibition of miR-23b-3p Ameliorates Scar-Like Phenotypes of Keloid Fibroblasts by Facilitating A20 Expression

Kuai¹,

Jian²

2022

CCID

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Purpose Accumulating evidence has reported that microRNAs (miRNAs) play a critical role in the mechanism of keloid formation, and recent research found that miR-23b-3p was upregulated in keloid fibroblasts (KFs). Herein, we explored the potential effect of miR-23b-3p on fibroblasts in keloid. Materials and Methods Clinical tissues, primary KFs and KEL FIB cells were used to detect the expression of miR-23b-3p by performing qRT-PCR. Gene knockdown was carried out to evaluate the molecular and biological changes of primary KFs and KEL FIB cells by conducting CCK-8 assay, flow cytometry and Western blot. The online databases and luciferase reporter assay were utilized to screen and identify the potential target of miR-23b-3p. Results Upregulation of miR-23b-3p was detected in keloid tissues, primary KFs and KF cell line KEL FIB cells, and inhibition of miR-23b-3p promoted apoptosis and suppressed proliferation and the expression of collagen I, collagen III and fibronectin of primary KFs and KEL FIB cells. Further investigation revealed that TNFAIP3 , the ubiquitin-editing enzyme A20, was the direct target of miR-23b-3p, and inhibition of miR-23b-3p promoted the expression of A20 in primary KFs and KEL FIB cells. The in vitro assays indicated that A20 suppression inhibited apoptosis and facilitated proliferation and the expression of collagen I, collagen III and fibronectin of miR-23b-3p inhibitor-transfected primary KFs and KEL FIB cells. Finally, we found that miR-23b-3p inhibitor reduced the expression of receptor interacting serine/threonine protein kinase 1 (RIPK1), which was partially reversed by A20 inhibition. Conclusion These findings suggested that inhibition of miR-23b-3p/A20/RIPK1 axis induced apoptosis, limited proliferation and decreased extracellular matrix of KFs, providing a potential therapeutic target for treatment of keloid.

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miR-194-5p serves a suppressive role in human keloid fibroblasts via targeting NR2F2

Cited by 12 publications

References 35 publications

microRNA-194 is increased in polycystic ovary syndrome granulosa cell and induce KGN cells apoptosis by direct targeting heparin-binding EGF-like growth factor

microRNA-194 is increased in polycystic ovary syndrome granulosa cell and induce KGN cells apoptosis by direct targeting heparin-binding EGF-like growth factor

The epigenetics of keloids

Inhibition of miR-23b-3p Ameliorates Scar-Like Phenotypes of Keloid Fibroblasts by Facilitating A20 Expression

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