Long Non-Coding RNAs in Oral Submucous Fibrosis: Their Functional Mechanisms and Recent Research Progress

He, Yaodong; Wang, Wei; Jiang, Pingping; Yuan, Lin; Guo, Qi; Xiang, Junwei; Gao, Yali; Wang, Yuanyin; Chen, Ran

doi:10.2147/jir.s337014

Cited by 5 publications

(4 citation statements)

References 125 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, studies of lncRNAs in the occurrence and malignant progression of OSF are still in nascent. To date, only 8 lncRNAs have been found to be related to the pathogenesis of OSF [ 38 ], including H19 [ 39 ], LINC00084 [ 40 ], HIF1A-AS1 [ 13 ], LINC00312 [ 12 ], LINC00974 [ 11 ], HOTTIP [ 41 ], GAS5-AS1 [ 10 ] and ADAMTS9-AS2 [ 15 ]. These lncRNAs are involved in the pathogenesis of OSF mainly by regulating myofibroblast activation [ 10 – 13 , 39 – 41 ] and epithelial to mesenchymal transition (EMT) [ 40 ].…”

Section: Discussionmentioning

confidence: 99%

Low LINC02147 expression promotes the malignant progression of oral submucous fibrosis

Liu

Xie

2022

BMC Oral Health

View full text Add to dashboard Cite

Background Key lncRNAs associated with the malignant progression of oral submucous fibrosis (OSF) to oral squamous cell carcinoma (OSCC) were identified. Methods Key lncRNAs with sequential changes from normal oral mucosa (NOM) to OSF to OSCC were identified based on the GEO database. Kaplan–Meier analysis was used to screen lncRNAs related to OSCC prognosis. Cox regression analysis was used to validate the independent prognostic value. qPCR was used to confirm the expression of the candidate lncRNAs. Gene set enrichment analysis (GSEA), nucleocytoplasmic separation assay, fluorescence in situ hybridization, RNA knockdown, western blot, and cell viability assay were performed to investigate the biological functions of the candidate lncRNA. A nomogram was constructed to quantitatively predict OSCC prognosis based on TCGA. Results Bioinformatics methods indicated that LINC02147 was sequentially downregulated from NOM to OSF to OSCC, as confirmed by clinical tissues and cells. Meanwhile, low LINC02147 expression, as an independent prognostic factor, predicted a poor prognosis for OSCC. GSEA and in vitro studies suggested that low LINC02147 expression promoted OSF malignant progression by promoting cell proliferation and differentiation. A LINC02147 signature-based nomogram successfully quantified each indicator’s contribution to the overall survival of OSCC. Conclusions Low LINC02147 expression promoted OSF malignant progression and predicted poor OSCC prognosis.

show abstract

Section: Discussionmentioning

confidence: 99%

Low LINC02147 expression promotes the malignant progression of oral submucous fibrosis

Liu

Xie

2022

BMC Oral Health

View full text Add to dashboard Cite

show abstract

“…Arecoline treatment decreased the transcription of miR-200c in buccal mucosal fibroblasts. 40 MiR-200c and miR-200b, which target ZEB1 and ZEB2 respectively, upregulate E-cadherin. ZEB1 interacts with the regulator of α-smooth muscle actin (α-SMA) and causes the upregulation of α-SMA in myofibroblasts during fibrogenesis.…”

Section: Osmf Tissue Non-coding Gene Biomarkersmentioning

confidence: 99%

Oral Submucosal Fibrosis: A Potentially Malignant Condition to be Considered

et al. 2023

View full text Add to dashboard Cite

A fatal disorder named oral submucous fibrosis (OSMF) is marked by the oral submucosa's progressive fibrosis. OSMF is distinguished by aberrant collagen deposition. In 1.5-15% of patients, it's a precancerous condition that progresses to a malignant tumour. Although nutrient deficiencies and immunological procedures could perform a role in pathogenesis, epidemiological evidence suggests that betel nut quid (which contains guvacine, arecoline, guvacoline, arecaidine, and chavibetol) contains areca nut, slaked lime, tobacco, is a significant risk factor for OSMF. Submucous fibrosis, xerostomia, ulceration, a burning sensation, and a limited mobility of the mouth are among the symptoms. The patient's quality of life is seriously affected by each of these components. The present article gives a broad overview of OSMF from a molecular viewpoint and describes what has been learned about its underlying causes, methods of diagnosis, and available treatments. Along with active therapy for OSMF, prophylaxis is essential, and this section gives a quick review of its treatment.

show abstract

“…Oral submucous fibrosis (OSF) is related to an elevated risk of malignancy (Liu et al, 2022; Patil et al, 2022). It is characterized by fibroelastic changes in oral mucosa and could gradually affect oral cavity muscles (He et al, 2021; Li & Cheng, 2022). In particular, studies have shown that chewing areca nut can induce the etiology and progression of OSF (Lee et al, 2021; Yu et al, 2021).…”

Section: Introductionmentioning

confidence: 99%

DNA methyltransferase 3A induces the occurrence of oral submucous fibrosis by promoting the methylation of the von Hippel–Lindau

Kuang,

Yang,

et al. 2023

Oral Diseases

View full text Add to dashboard Cite

BackgroundOral submucous fibrosis (OSF) is associated with malignant disorders. DNA methyltransferase 3A (DNMT3A) is a DNA methylesterase reported to be upregulated in multiple organs and shown to inhibit fibrosis. However, the detailed effect of DNMT3A on OSF remains unclear.MethodsTo mimic OSF in vitro, oral fibroblasts were exposed to arecoline and molecular biological experiments were performed to detect the function of DNMT3A in OSF.ResultsWe found that von Hippel–Lindau (VHL) was downregulated and highly methylated in OSF. Arecoline remarkably increased the viability, invasiveness, and migration of oral fibroblasts, but upregulation of VHL partially reversed these effects. DNMT3A induces DNA hypermethylation in the VHL promoter, and VHL markedly inhibits the level of tenascin‐C (TNC) by inducing the ubiquitination of TNC. TNC reversed the inhibitory effect of VHL upregulation on the differentiation of oral fibroblasts into myofibroblasts.ConclusionDNMT3A induces OSF by promoting methylation of the VHL promoter. Hence, our study provides novel insights into the discovery of novel strategies that can be employed against OSF.

show abstract

Long Non-Coding RNAs in Oral Submucous Fibrosis: Their Functional Mechanisms and Recent Research Progress

Cited by 5 publications

References 125 publications

Low LINC02147 expression promotes the malignant progression of oral submucous fibrosis

Low LINC02147 expression promotes the malignant progression of oral submucous fibrosis

Oral Submucosal Fibrosis: A Potentially Malignant Condition to be Considered

DNA methyltransferase 3A induces the occurrence of oral submucous fibrosis by promoting the methylation of the von Hippel–Lindau

Contact Info

Product

Resources

About