Journal of Prevention and Treatment for Stomatological Diseases ›› 2020, Vol. 28 ›› Issue (11): 733-738.doi: 10.12016/j.issn.2096-1456.2020.11.010

• Review Articles • Previous Articles     Next Articles

Role and mechanism of microRNAs in oral lichen planus

YANG Yijie(),GE Shuyun()   

  1. Shanghai Key Laboratory of Stomatology & Shanghai Research institute of Stomatology, shanghai 200011, China
  • Received:2019-12-15 Revised:2020-04-14 Online:2020-11-20 Published:2020-09-29
  • Contact: Shuyun GE E-mail:18516375537@163.com;imyun@sina.com

Abstract:

Oral lichen planus (OLP) is a chronic inflammatory disease of the mucosa, some of which will develop into oral squamous cell carcinoma (OSCC). However, the pathogenesis of OLP remains unknown, but autoimmunity has been suggested as a potential cause. MicroRNAs (miRNAs), which are small noncoding RNAs, have been reported to be involved in a series of physiological events as well as the progression of diseases. The evidence indicates that miRNAs may be highly related to both the initiation and malignant progression of OLP. MiR-146a, miR-26b, miR-155, miR-19a and miR-125a are able to trigger OLP by regulating autoimmunity, and miR-137, miR-125b, and miR-27b may accelerate the carcinogenesis of OLP. These miRNAs may be potential targets for prognosis and treatment. Subsequent studies are expected to focus on a more comprehensive exploration of the role of miRNAs in OLP (including specific action pathways and other OLP-related miRNAs), as well as the potential for miRNAs to predict the treatment outcome of OLP. This review provides an updated summary of the roles of miRNAs in OLP to provide new ideas and approaches to OLP research.

Key words: oral lichen planus, precancerous condition, microRNA, autoimmunity, chronic inflammation, carcinogenesis, therapeutic targets

CLC Number: 

  • R781.5

Figure 1

Roles of miRNAs in oral lichen planus Foxp3: forked head transcription factor 3; TRAF6: forked head transcription factor 3; COX-2: cyclooxygenase-2; eNOS: endothelial nitric oxide synthase; TLR2: Toll-like receptor; IL: interleukin; TNF-α: tumor necrosis factor-α; IFN-γ: interferon-γ; Th1/Th2: helper T cells 1/helper T cells 2; CCL5: CC chemokine ligand 5; CCR5: chemokine receptor 5; T: T cells; PI3K: phosphatidylinositol 3-kinase; Akt: protein kinase B; mTOR: mammalian target of rapamycin; MMP-2: matrix metalloproteinase-2; PLK2: polo-like kinase 2; OLP: oral lichen planus"

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