miR-4417 suppresses keloid fibrosis growth by inhibiting CyclinD1

Liu, Pei; Hu, Yaotian; Lin, Xia; Du, Min; Hu, Zhensheng

doi:10.1007/s12038-020-0018-9

Cited by 10 publications

(10 citation statements)

References 26 publications

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“…info Table S1, row 45). 114 All this evidence suggests that miRNAs function as important regulators in keloid formation by regulating post-transcriptional translation and mediating downstream target genes, mainly influencing cell behaviours and ECM production, playing key roles in the pathogenesis of keloids.…”

Section: Inverse Correlation Of Expression Between Mirna-205-5p Andmentioning

confidence: 99%

“…Pathways related to cell division, proliferation and tumour suppression have been found to have multiple types of altered epigenetic modulation in keloids. Genes involved in this process have been shown to have aberrant DNA methylation, 22,[55][56][57]59 altered histone acetylation patterns, 58,64 miRNAs 65,76,[78][79][80]82,[102][103][104][105]107,109,110,[112][113][114] and lncRNAs. [119][120][121][124][125][126][129][130][131]136,138 This multitude of epigenetic modifications result in the excess cell division and proliferation by both stimulating promoters and blocking repressors of this process.…”

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

confidence: 99%

“…Genes involved in the process of apoptosis have also been shown to have aberrant epigenetic status, including modifications to histone acetylation, 62,64 miRNAs 79,80,93,94,96,103,107,[109][110][111]114 and lncRNAs. 120,126,131,136,138 The lack of appropriate apoptotic signals contributes to the excessive number and abnormal phenotype of cells in keloid scars.…”

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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Section: Inverse Correlation Of Expression Between Mirna-205-5p Andmentioning

confidence: 99%

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

confidence: 99%

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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“…A potential therapeutic target in keloids [81] miR-1-3p and miR-214-5p Downregulation TM4SF1 MiR-1-3p and miR-214-5p inhibited cell proliferation, migration, and induced apoptosis in HKFs A potential targets in therapies for keloids [82] lncRNA-H19 Upregulation miR-29a LncRNA-H19 affected the viability and apoptosis of KFs through COL1A1 signaling…”

Section: Conclusion and Future Perspectivesmentioning

confidence: 99%

“…The increased expression of miR-188-5p transfected with miR-188-5p mimic exerted an inhibitory effect on the regulation of proliferation, migration, and invasion in KFs by restraining PI3K/Akt/MMP-2/9 signaling pathway [ 80 ]. Liu et al determined that miR-4417 was significantly down-regulated in keloid tissue and KFs, and increased miR-4417 expression led to the suppression of KFs proliferation and whereas miR-4417 depletion exerted an opposite effect, inferring the implication of miR-4417/CyclinD1 axis in keloid [ 81 ]. The overexpression of miR-1-3p/miR-214-5p could suppress the proliferation, migration, and invasion of human KFs, and promote apoptosis through AKT/ERK signaling pathway [ 82 ].…”

Section: Epigenetic Modification Mechanisms In Keloidmentioning

confidence: 99%

Epigenetic modification mechanisms involved in keloid: current status and prospect

Ren

Hou

et al. 2020

Clin Epigenet

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Keloid, a common dermal fibroproliferative disorder, is benign skin tumors characterized by the aggressive fibroblasts proliferation and excessive accumulation of extracellular matrix. However, common therapeutic approaches of keloid have limited effectiveness, emphasizing the momentousness of developing innovative mechanisms and therapeutic strategies. Epigenetics, representing the potential link of complex interactions between genetics and external risk factors, is currently under intense scrutiny. Accumulating evidence has demonstrated that multiple diverse and reversible epigenetic modifications, represented by DNA methylation, histone modification, and non-coding RNAs (ncRNAs), play a critical role in gene regulation and downstream fibroblastic function in keloid. Importantly, abnormal epigenetic modification manipulates multiple behaviors of keloid-derived fibroblasts, which served as the main cellular components in keloid skin tissue, including proliferation, migration, apoptosis, and differentiation. Here, we have reviewed and summarized the present available clinical and experimental studies to deeply investigate the expression profiles and clarify the mechanisms of epigenetic modification in the progression of keloid, mainly including DNA methylation, histone modification, and ncRNAs (miRNA, lncRNA, and circRNA). Besides, we also provide the challenges and future perspectives associated with epigenetics modification in keloid. Deciphering the complicated epigenetic modification in keloid is hopeful to bring novel insights into the pathogenesis etiology and diagnostic/therapeutic targets in keloid, laying a foundation for optimal keloid ending.

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