Differential Expression Profiles and Difference Analysis of MicroRNAs in Tissues of Patients with Oral Lichen Planus were Screened by High-throughput Sequencing

doi:10.13701/j.cnki.kqyxyj.2022.08.014

Abstract

Abstract: Objective: To explore the role of microRNAs (miRNAs) in the pathogenesis of oral lichen planus (OLP). Methods: The tissues of 3 OLP patients (experimental group) and 3 normal individual (control group) were collected in the Department of Stomatology of the Fourth Hospital of Hebei Medical University for illumina high-throughput sequencing to screen the differentially expressed miRNAs. The target genes were predicted and analyzed by bioinformatics analyses. Results: A total of 61 differentially expressed miRNAs were screened between the two groups by using DESeq software, including 23 up-regulated and 38 down-regulated miRNAs. Three of the most significantly up-regulated (miR-449c-5p, miR-663b, and miR-196a-5p) and down-regulated (miR-133b, miR-1-3p, and miR-133a-3p) miRNAs were selected for target gene prediction, and GO analysis revealed that these targets were mainly enriched in the cell membrane region and might be involved in biological processes such as cell migration, differentiation, metabolism, and secretion regulation. KEGG analysis revealed that these targets were significantly enriched in MAPK, Rap1, NF-κB, Ras, and other signaling pathways. Conclusion: There are differentially expressed miRNAs between OLP and normal oral mucosa, and these miRNAs can act on MAPK, NF-κB, Rap1 and other pathways through SEMA3F, HECW1, POLDIP and other target genes to participate in the development and progression of OLP.

Key words: oral lichen planus, high-throughput nucleotide sequencing, microRNAs, bioinformatics analyses

LIU Jian, LI Tiancui, WU Jingjing, YAO Manman, XU Yanzhi, LI Jingzhe. Differential Expression Profiles and Difference Analysis of MicroRNAs in Tissues of Patients with Oral Lichen Planus were Screened by High-throughput Sequencing[J]. Journal of Oral Science Research, 2022, 38(8): 768-772.

References

[1] Cheng YL, Gould A, Kurago Z, et al. Diagnosis of oral lichen planus: a position paper of the American Academy of Oral and Maxillofacial Pathology [J]. Oral Surg Oral Med Oral Pathol Oral Radiol, 2016, 122(3):332-354.
[2] Wang L, Wu W, Chen J, et al. MicroRNA microarray-based identification of involvement of miR-155 and miR-19a in development of oral lichen planus (OLP) by modulating Th1/Th2 balance via targeting eNOS and toll-like receptor 2 (TLR2) [J]. Med Sci Monit, 2018, 24:3591-3603.
[3] Ma H, Wu Y, Yang H, et al. MicroRNAs in oral lichen planus and potential miRNA-mRNA pathogenesis with essential cytokines: a review [J]. Oral Surg Oral Med Oral Pathol Oral Radiol, 2016, 122(2):164-173.
[4] 高胜男, 李言君, 李建卫, 等.糜烂型口腔扁平苔藓差异表达MicroRNAs的筛选[J].实用口腔医学,2019,35(5):696-700.
[5] Laeijendecker R, van Joost T, Kuizinga MC, et al. Premalignant nature of oral lichen planus [J]. Acta Derm Venereol, 2005, 85(6):516-520.
[6] González-Moles MÁ, Ramos-García P, Warnakulasuriya S. An appraisal of highest quality studies reporting malignant transformation of oral lichen planus based on a systematic review [J]. Oral Dis, 2021, 27(8):1908-1918.
[7] Clague J, Lippman SM, Yang H, et al. Genetic variation in MicroRNA genes and risk of oral premalignant lesions [J]. Mol Carcinog, 2010, 49(2):183-189.
[8] Sun X, Zhang H. miR-451 elevation relieves inflammatory pain by suppressing microglial activation-evoked inflammatory response via targeting TLR4 [J]. Cell Tissue Res, 2018, 374(3):487-495.
[9] Quero L, Tiaden AN, Hanser E, et al. miR-221-3p drives the shift of M2-macrophages to a pro-inflammatory function by suppressing JAK3/STAT3 activation [J]. Front Immunol, 2019, 10:3087.
[10] 曹直.miR-155在口腔扁平苔藓患者外周血及组织中表达及意义[J].口腔医学研究,2016,32(2):185-188.
[11] Chang Y, Chen X, Tian Y, et al. Downregulation of microRNA-155-5p prevents immune thrombocytopenia by promoting macrophage M2 polarization via the SOCS1-dependent PD1/PDL1 pathway [J]. Life Sci, 2020, 257:118057.
[12] Louafi F, Martinez-Nunez RT, Sanchez-Elsner T. MicroRNA-155 targets SMAD2 and modulates the response of macrophages to transforming growth factor-{beta} [J]. J Biol Chem, 2010, 285(53):41328-41336.
[13] Gwiggner M, Martinez-Nunez RT, Whiteoak SR, et al. MicroRNA-31 and microRNA-155 are overexpressed in ulcerative colitis and regulate IL-13 signaling by targeting interleukin 13 receptor α-1 [J]. Genes (Basel), 2018, 9(2):85.
[14] Tao Y, Ai R, Hao Y, et al. Role of miR-155 in immune regulation and its relevance in oral lichen planus [J]. Exp Ther Med, 2019,17(1):575-586.
[15] Matos LL, Menderico JG, Theodoro TR, et al. Cancer-associated fibroblast regulation by microRNAs promotes invasion of oral squamous cell carcinoma [J]. Oral Oncol, 2020, 110:104909.
[16] 浦光瑞, 张虹.口腔扁平苔藓中MMP-2和MMP-9的表达及意义[J].大连医科大学学报,2012,34(5):446-449.
[17] Gao X, Han D, Fan W. Down-regulation of RBP-J mediated by microRNA-133a suppresses dendritic cells and functions as a potential tumor suppressor in osteosarcoma [J]. Exp Cell Res, 2016, 349(2):264-272.
[18] Meng Z, Zhang H, Li L, et al. Clinical significance of miR-142-3p in oral lichen planus and its regulatory role in keratinocyte proliferation [J]. Oral Surg Oral Med Oral Pathol Oral Radiol, 2021, 132(4):441-447.
[19] Wang J, Luo H, Xiao Y, et al. miR-125b inhibits keratinocyte proliferation and promotes keratinocyte apoptosis in oral lichen planus by targeting MMP-2 expression through PI3K/Akt/mTOR pathway [J]. Biomed Pharmacother, 2016, 80:373-380.
[20] Gholizadeh N, Emami RA, Mohammadpour H, et al. Association of MAPK and its regulatory miRNAs (603, 4301, 8485, and 4731) with the malignant transformation of oral lichen planus [J]. Mol Biol Rep, 2020, 47(2):1223-1232.
[21] Jiang C, Wei W, Wang Y, et al. TRIM21 causes abnormal expression of IL-6 in oral lichen planus via the TRIB2-MAPK signal axis [J]. Am J Transl Res, 2020, 12(8):4648-4658.
[22] Smith S, Ní GJ, McCarthy E, et al. Estrogen receptor α regulates tripartite motif-containing protein 21 expression, contributing to dysregulated cytokine production in systemic lupus erythematosus [J]. Arthritis Rheumatol, 2014, 66(1):163-172.
[23] Deng S, Xu Y, Wang X, et al. Study on the role of salivary flora and NF-κB inflammatory signal pathway in oral lichen planus [J]. Inflammation, 2020, 43(3):994-1008.