Wnt Signaling Pathway in Oral Lesions

Ejaz, Iqra; Ghafoor, Sarah

doi:10.5455/jpma.5890

Cited by 10 publications

(14 citation statements)

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“…β‐catenin is a key molecular of the Wnt signaling pathway, which is one of the essential cascades in the periodontium, and plays a role in cell growth, differentiation, and survival (Clevers & Nusse, 2012). Ejaz I et al reported that regulation of Wnt signaling pathway, such as reintroduction of Wnt antagonists, in periapical lesions restricted the pathological bone loss in periapical and periodontal lesions (Ejaz & Ghafoor, 2019). Aberrantly elevated Wnt signaling is responsible for cementum overgrowth and dental ankyloses (Wu et al., 2019).…”

Section: Discussionmentioning

confidence: 99%

Long non‐coding RNA TUG1 participates in LPS‐induced periodontitis by regulating miR‐498/RORA pathway

Huang

Sun

et al. 2020

Oral Diseases

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Aim This study was aimed to investigate the role of TUG1 in LPS‐stimulated hPDLCs and to evaluate the potential functions of TUG1 in the pathogenesis of periodontitis. Methods LPS‐stimulated hPDLCs were established as the cell model. CCK‐8 assay was performed to assess cell proliferation ability. Flow cytometry was performed to detect cell cycle distribution, and quantitative RT‐PCR and Western blotting were conducted to measure gene expressions. ELISA kits were used to evaluate the production of inflammatory cytokines. The putative binding site between TUG1 and miR‐498 was verified using luciferase reporter and RNA immunoprecipitation assays. Results TUG1 was downregulated upon LPS stimulation in hPDLCs. TUG1 overexpression promoted cell proliferation through regulating the cell cycle distribution, along with the decreased expression of p21 and increased expression of CDK2 and cyclin D1. Besides, TUG1 overexpression decreased the production of inflammatory cytokines. The effects were opposite upon TUG1 knockdown. TUG1 negatively regulated its target miR‐498, and influenced the expression of RORA, the direct target of miR‐498. Simultaneous TUG1 overexpression and miR‐498 reversed the effect of TUG1 overexpression alone on alleviating LPS‐induced cell injury and inhibition of Wnt/β‐catenin signaling, which was further changeover after co‐overexpression with RORA. Conclusion Therefore, TUG1 could protect against periodontitis via regulating miR‐498/RORA mediated Wnt/β‐catenin signaling.

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Section: Discussionmentioning

confidence: 99%

Long non‐coding RNA TUG1 participates in LPS‐induced periodontitis by regulating miR‐498/RORA pathway

Huang

Sun

et al. 2020

Oral Diseases

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“…It plays an intrinsic role in cell proliferation, differentiation, regeneration, and some other cellular functions. [23] When cells receive Wnt signal, β-catenin protein will be stably accumulated in the cytoplasm, transferred to the nucleus, and then regulate the expression of downstream target genes; without Wnt protein stimulation, β-catenin protein will be degraded by proteasome through activated multiple proteins degradation complex. [24] Mutation of related genes in the Wnt/β-catenin signaling pathway will lead to abnormal regulation of Wnt/β-catenin signaling pathway.…”

Section: Discussionmentioning

confidence: 99%

Microsatellite instability/mismatch repair deficiency and activation of the Wnt/β-catenin signaling pathway in gastric adenocarcinoma of the fundic gland: A case report

Yang

2022

Medicine

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Rationale: Gastric adenocarcinoma of the fundic gland is a rare, well-differentiated variant of gastric adenocarcinoma, which has been proposed as a novel disease entity. As a result of mismatch repair deficiency, microsatellite instability has been frequently observed in various human cancers and widely performed in the area of cancer pathogenesis. Herein, we report a case of gastric adenocarcinoma of fundic gland presented with microsatellite instability phenotype. Patient concerns: A 46-year-old man was referred to our hospital for abdominal distension and pain. Diagnosis: The patient contained 3 tumor lesions with different degrees of histologic differentiation and microsatellite instability. The lesions were located in the upper third of the stomach. The tumor size was 55 mm. Macroscopically, tumor showed an ulcerative type. In terms of depth of invasion, tumor lesion invaded into subserosa with lymphatic invasion. In addition, this patient did not present GNAS mutation but harbored AXIN2 mutation. By immunohistochemistry, the expression level of β-catenin protein in the nucleus of the carcinoma cells was obviously higher than that in normal nucleus. Compared with microsatellite instability-low lesion, PD-1, PD-L1, and CD8 were positive in the microsatellite instability-high lesions. Interventions: The patient underwent surgical resection and postoperative chemotherapy. Outcomes: The patient experienced distant metastasis and died from severe complications after 6 months of treatment. Lessons: These results suggested that the mutation of Wnt component genes associated with Wnt/β-catenin signaling pathway activation may play a role in promoting the occurrence of gastric adenocarcinoma of fundic gland. This is the first report of a gastric adenocarcinoma of fundic gland with microsatellite instability. These findings modify our understanding of the pathophysiology of gastric adenocarcinoma of fundic gland.

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“… 38 It is known that CCND1 is a target of the WNT signaling pathway, which has been reported to have a significant role in malignant transformation of oral lesions such as OLP, and contribute to the chronic inflammatory disease. 39 Accordingly, we speculated that miR-23a-3p might inhibit keratinocyte proliferation and inflammatory response via targeting CCND1. However, the underlying mechanism is worthy of exploration.…”

Section: Discussionmentioning

confidence: 99%

Clinical Values of miR-23a-3p in Oral Lichen Planus and Its Role in Keratinocyte Proliferation and Inflammatory Response

Wang¹,

Hu²,

Li³

2021

JIR

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Purpose Oral lichen planus (OLP) is a chronic inflammatory disease occurring in the oral cavity, and several miRNAs have been identified to be involved in the disease progression and malignant transformation. This study investigated the expression changes of miR-23a-3p in OLP patients, and further explored its functional role in keratinocyte cell proliferation and inflammatory response. Patients and Methods Fifty buccal mucosal tissue samples were collected from OLP patients. HaCaT cells were cultured with lipopolysaccharides (LPS) to mimic the condition of OLP in vitro. RNA extraction and quantitative real-time PCR (qRT-PCR) were used for the measurement of miR-23a-3p levels. The cell viability and inflammation were detected by using cell counting kit-8 (CCK-8) and enzyme-linked immunosorbent assay (ELISA). The target gene of miR-23a-3p was verified by using luciferase reporter assay. Results Compared with the control group, miR-23a-3p was significantly downregulated in the buccal mucosal tissues of OLP patients, and a remarkably decreased level of miR-23a-3p was detected in patients with erosive OLP. ROC curve demonstrated the diagnostic value of miR-23a-3p for OLP with the AUC of 0.908, it can also distinguish erosive OLP from the non-erosive ones. MiR-23a-3p level was negatively associated with RAE (reticular, atrophic, erosive) score in OLP patients (r = −0.790, P < 0.001). The in vitro experiments indicated that overexpression of miR-23a-3p reversed the promotive effect of LPS on HaCaT cell proliferation and reduced the protein levels of TNF-α and IL-6. The cyclin D1 (CCND1) was a direct target gene of miR-23a-3p, it was overexpressed in OLP cell models. Conclusion MiR-23a-3p was at the low expression in OLP patients and showed close association with the disease severity. Overexpression of miR-23a-3p might inhibit keratinocyte proliferation and inflammatory response via targeting CCND1.

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Wnt Signaling Pathway in Oral Lesions

Cited by 10 publications

References 0 publications

Long non‐coding RNA TUG1 participates in LPS‐induced periodontitis by regulating miR‐498/RORA pathway

Long non‐coding RNA TUG1 participates in LPS‐induced periodontitis by regulating miR‐498/RORA pathway

Microsatellite instability/mismatch repair deficiency and activation of the Wnt/β-catenin signaling pathway in gastric adenocarcinoma of the fundic gland: A case report

Clinical Values of miR-23a-3p in Oral Lichen Planus and Its Role in Keratinocyte Proliferation and Inflammatory Response

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