Potential role of long non-coding RNA (nuclear paraspeckle assembly transcript 1 and metastasis associated lung adenocarcinoma transcript 1) in periodontitis pathogenesis: A systematic review
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Abstract
Background: Dysregulation of Long non-coding (lnc)RNAs has been linked to periodontitis, with potential importance in disease onset and progression. These lncRNAs potentially modulate inflammatory/immune responses during periodontitis. This review aimed to highlight the potential role of Nuclear Paraspeckle Assembly Transcript (NEAT)1 and Metastasis Associated Lung Adenocarcinoma Transcript (MALAT)1 lncRNAs in periodontitis pathogenesis. Methods: A literature search of three electronic databases was performed in SCOPUS, MEDLINE (PubMed) and EMBASE using search terms linking periodontitis/periodontal disease with NEAT1 and MALAT1 lncRNAs. Duplicate publications were removed from the retrieved articles which were then filtered to include the most relevant papers for evidence synthesis. Results: Nine studies (in vitro and in vivo) were included in the final analysis. The total number of studies investigating the role of NEAT1 and MALAT1 in pathogenesis of periodontitis was 4 and 5, respectively. The findings indicated gene expression changes of NEAT1 and MALAT1 in periodontitis compared with periodontal health. Conclusion: No concrete evidence could be withdrawn from this review; however, results suggested that lncRNAs, NEAT1 and MALAT1 could be involved in periodontitis pathogenesis. However, further in vivo studies are required to confirm these findings.
Received date: 20-03-2024
Accepted date: 01-05-2024
Published date: 15-12-2024
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References
Luchian I, Moscalu M, Goriuc A, Nucci L, Tatarciuc M, Martu I, et al. Using Salivary MMP-9 to Successfully Quantify Periodontal Inflammation during Orthodontic Treatment. J Clin Med. 2021;10(3):1-9.
Genco RJ, Borgnakke WS. Risk factors for periodontal disease. Periodontol 2000. 2013;62(1):59-94.7
Arigbede AO, Babatope BO, Bamidele MK. Periodontitis and systemic diseases: A literature review. J Indian Soc Periodontol. 2012;16(4):487-91.
Abdellah Z, Ahmadi A, Ahmed S, Aimable M, Ainscough R, Almeida J, et al. Finishing the euchromatic sequence of the human genome. Nature. 2004;431(7011):931-45.
Ulveling D, Francastel C, Hubé F. When one is better than two: RNA with dual functions. Biochimie. 2011;93(4):633-44.
Kapranov P, Cheng J, Dike S, Nix DA, Duttagupta R, Willingham AT, et al. RNA maps reveal new RNA classes and a possible function for pervasive transcription. Science. 2007;316(5830):1484-8.
Li X, Wu Z, Fu X, Han W. lncRNAs: insights into their function and mechanics in underlying disorders. Mutat Res Rev Mutat Res. 2014;762:1-21.
Wang H, Radomska HS, Phelps MA, Iorns E, Tsui R, Denis A, et al. Replication study: Coding-independent regulation of the tumor suppressor pten by competing endogenous mRNAs. eLife. 2020;9:1-19.
Yoon J-H, Abdelmohsen K, Gorospe M, editors. Functional interactions among microRNAs and long noncoding RNAs. Seminars in cell & developmental biology; 2014: Elsevier.
Wang Y, Wu C, Zhang C, Li Z, Zhu T, Chen J, et al. TGF-β-induced STAT3 overexpression promotes human head and neck squamous cell carcinoma invasion and metastasis through malat1/miR-30a interactions. Cancer Lett. 2018;436:52-62.
Battistelli C, Cicchini C, Santangelo L, Tramontano A, Grassi L, Gonzalez FJ, et al. The Snail repressor recruits EZH2 to specific genomic sites through the enrollment of the lncRNA HOTAIR in epithelial-to-mesenchymal transition. Oncogene. 2017;36(7):942-55.
Zou Y, Li C, Shu F, Tian Z, Xu W, Xu H, et al. LncRNA Expression Signatures in Periodontitis Revealed by Microarray: The Potential Role of lncRNAs in Periodontitis Pathogenesis. J Cell Biochem. 2015;116(4):640-7.
Sayad A, Mirzajani S, Gholami L, Razzaghi P, Ghafouri-Fard S, Taheri M. Emerging role of long non-coding RNAs in the pathogenesis of periodontitis. Biomed Pharmacother. 2020;129.
Walther K, Schulte LN. The role of lncRNAs in innate immunity and inflammation. RNA Biol. 2021;18(5):587-603.
Zhang L, Lv H, Cui Y, Shi R. The role of long non-coding RNA (lncRNA) nuclear paraspeckle assembly transcript 1 (NEAT1) in chronic periodontitis progression. Bioengineered. 2022;13(2):2336-45.
Qi Y, Fei Y, Wang J, Wang D. Expression level and clinical significance of NEAT1 in patients with chronic periodontitis. J Dent Sci. 2022.
Hu W, Lei X, Luo J, Gou X. Impacts of long noncoding RNA MALAT1 on LPS-induced periodontitis via modulating miR-155/SIRT1 axis. Turk J Biochem. 2022;47(5):595-601.
Chen Q, Cao M, Ge H. Knockdown of MALAT1 Inhibits the Progression of Chronic Periodontitis via Targeting miR-769-5p/HIF3A Axis. Biomed Res Int. 2021;2021.
Li J, Wang M, Song L, Wang X, Lai W, Jiang S. LncRNA MALAT1 regulates inflammatory cytokine production in lipopolysaccharide-stimulated human gingival fibroblasts through sponging miR-20a and activating TLR4 pathway. J Periodontal Res. 2020;55(2):182-90.
Li S, Liu X, Li H, Pan H, Acharya A, Deng Y, et al. Integrated analysis of long noncoding RNA-associated competing endogenous RNA network in periodontitis. J Periodontal Res. 2018;53(4):495-505.
Zhang T, Yang K, Chen Y, Jiang Y, Zhou Z, Liu J, et al. Impaired autophagy flux by lncRNA NEAT1 is critical for inflammation factors production in human periodontal ligament stem cells with nicotine treatment. J Periodontal Res. 2023;58(1):70-82.
Sayad A, Ghafouri-Fard S, Shams B, Arsang-Jang S, Gholami L, Taheri M. Blood and tissue levels of lncRNAs in periodontitis. J Cell Physiol. 2020;235(12):9568-76.
Ahmad I, Naqvi RA, Valverde A, Naqvi AR. LncRNA MALAT1/microRNA-30b axis regulate macrophage polarization and function. bioRxiv. 2023.
Gholami L, Ghafouri-Fard S, Mirzajani S, Arsang-Jang S, Taheri M, Dehbani Z, et al. The lncRNA ANRIL is down-regulated in peripheral blood of patients with periodontitis. Noncoding RNA Res. 2020;5(2):60-6.
Li J, Wang M, Song L, Wang X, Lai W, Jiang S. Lnc RNA MALAT 1 regulates inflammatory cytokine production in lipopolysaccharide‐stimulated human gingival fibroblasts through sponging miR‐20a and activating TLR 4 pathway. J Periodontal Res. 2020;55(2):182-90.
Atarchi AR. Potential of Salivary Matrix Metalloproteinase 9 to Discriminate Periodontal health and disease. J Bagh Coll Dent. 2022;34(2):74-9.
Li JS, Xie YF, Song LT, Wang XP, Jiang SY. Expression profile of long non-coding RNA in the gingival tissue from patient with aggressive periodontitis. Zhonghua kou qiang yi xue za zhi = Zhonghua kouqiang yixue zazhi = Chinese J stomatol. 2018;53(9):635-9.
Jin SH, Zhou RH, Guan XY, Zhou JG, Liu JG. Identification of novel key lncRNAs involved in periodontitis by weighted gene co-expression network analysis. J Periodontal Res. 2020;55(1):96-106.
Abdulkareem AA, Shelton RM, Landini G, Cooper PR, Milward MR. Potential role of periodontal pathogens in compromising epithelial barrier function by inducing epithelial-mesenchymal transition. J Periodontal Res. 2018;53(4):565-74.
Yang J, Antin P, Berx G, Blanpain C, Brabletz T, Bronner M, et al. Guidelines and definitions for research on epithelial–mesenchymal transition. Nat Rev Mol Cell Biol. 2020;21(6):341-52.
Rubinstein MR, Wang X, Liu W, Hao Y, Cai G, Han YW. Fusobacterium nucleatum promotes colorectal carcinogenesis by modulating E-cadherin/β-catenin signaling via its FadA adhesin. Cell Host Microbe. 2013;14(2):195-206.
Saliem SS, Bede SY, Abdulkareem AA, Abdullah BH, Milward MR, Cooper PR. Gingival tissue samples from periodontitis patients demonstrate epithelial-mesenchymal transition phenotype. J Periodontal Res. 2023;58(2):247-55.
Li Y, Guo W, Cai Y. NEAT1 Promotes LPS-induced Inflammatory Injury in Macrophages by Regulating MiR-17-5p/TLR4. Open Med (Wars). 2020;15:38-49.
Chen LJ, Li JM, Zhang WD, Liu W, Li XY, Ouyang B, et al. LncRNA NEAT1 activates MyD88/NF-κB pathway in bronchopneumonia through targeting miR-155-5p. Autoimmunity. 2021;54(2):104-13.
Ricciardi M, Zanotto M, Malpeli G, Bassi G, Perbellini O, Chilosi M, et al. Epithelial-to-mesenchymal transition (EMT) induced by inflammatory priming elicits mesenchymal stromal cell-like immune-modulatory properties in cancer cells. Br J Cancer. 2015;112(6):1067-75.
Li W, Cheng B. Knockdown of LncRNA NEAT1 inhibits myofibroblast activity in oral submucous fibrosis through miR-760/TPM1 axis. J Dent Sci. 2022;17(2):707-17.
He K, Gan WJ. Wnt/β-Catenin Signaling Pathway in the Development and Progression of Colorectal Cancer. Cancer Manag Res. 2023;15:435-48.
Zhang M, Weng W, Zhang Q, Wu Y, Ni S, Tan C, et al. The lncRNA NEAT1 activates Wnt/β-catenin signaling and promotes colorectal cancer progression via interacting with DDX5. J Hematol Oncol. 2018;11(1):113.
Sharma JR, Agraval H, Yadav UCS. Cigarette smoke induces epithelial-to-mesenchymal transition, stemness, and metastasis in lung adenocarcinoma cells via upregulated RUNX-2/galectin-3 pathway. Life Sci. 2023;318:121480.
Ma JJ, Liu HM, Xu XH, Guo LX, Lin Q. Study on gene expression patterns and functional pathways of peripheral blood monocytes reveals potential molecular mechanism of surgical treatment for periodontitis. World J Clin Cases. 2019;7(12):1383-92.
Zhang Z, Wen H, Peng B, Weng J, Zeng F. Downregulated microRNA-129-5p by Long Non-coding RNA NEAT1 Upregulates PEG3 Expression to Aggravate Non-alcoholic Steatohepatitis. Front genet. 2020;11:563265-.
He J, Zheng Z, Li S, Liao C, Li Y. Identification and assessment of differentially expressed necroptosis long non-coding RNAs associated with periodontitis in human. BMC oral health. 2023;23(1).
Zhou HJ, Wang LQ, Wang DB, Yu JB, Zhu Y, Xu QS, et al. Long noncoding RNA MALAT1 contributes to inflammatory response of microglia following spinal cord injury via the modulation of a miR-199b/IKKβ/NF-κB signaling pathway. Am J Physiol Cell Physiol. 2018;315(1):C52-c61.
Finoti LS, Nepomuceno R, Pigossi SC, Corbi SC, Secolin R, Scarel-Caminaga RM. Association between interleukin-8 levels and chronic periodontal disease: A PRISMA-compliant systematic review and meta-analysis. Medicine (Baltimore). 2017;96(22):e6932.
Al-Ghurabi BH, Mohssen SM. Salivary level of RANKL and OPG in chronic periodontitis. J Bagh Coll Dent. 2015;27(1):189-94.
Zhang C, Pan L, Zhang H, Ke T, Yang Y, Zhang L, et al. Osteoblasts-Derived Exosomal lncRNA-MALAT1 Promotes Osteoclastogenesis by Targeting the miR-124/NFATc1 Signaling Axis in Bone Marrow-Derived Macrophages. Int J Nanomedicine. 2023;18:781-95.
Peng C, Wang Y, Ji L, Kuang L, Yu Z, Li H, et al. LncRNA-MALAT1/miRNA-204-5p/Smad4 Axis Regulates Epithelial-Mesenchymal Transition, Proliferation and Migration of Lens Epithelial Cells. Curr Eye Res. 2021;46(8):1137