Odontogenic epithelial proliferation is correlated with COX-2 expression in dentigerous cyst and ameloblastoma

Alsaegh, Mohammed Amjed; Matsumoto, Hitoshi; Taniguchi, Takahiro; Zhu, Sheng

doi:10.3892/etm.2016.3939

Cited by 14 publications

(20 citation statements)

References 52 publications

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“…Wassem et al (16) concluded that activation and proliferation of keratinocytes result in downregulation of K15. Our previous studies showed the non-different expression of proliferating epithelial cells in OKC and AB (17,18). This may explain the similar expression of K15 in odontogenic epithelium of both OKC and AB in the current study.…”

Section: Discussionsupporting

confidence: 62%

“…The current study, as many previous reports (9)(10)(11)(12)15,17,18) excluded the use of control group samples in the study of odontogenic lesions. This is because no true tissue equivalent exists to serve as a negative control, as odontogenic lesions encompass reactive tissues and tumors which replace the healthy bone.…”

Section: Discussionmentioning

confidence: 99%

“…The expression and type of keratin is highly affected by epithelial cell differentiation and lineage (8). Therefore, expression of the keratins 1, 2, 4, 5,6,7,8,10,13,14,16,17,18,19 and 20 was investigated in odontogenic cysts and tumors (9)(10)(11)(12)(13)(14). To the best of our knowledge, there is only one study that discussed the expression of K15 in AB (15), and no presence of any previous literature that deals with K15 expression in other odontogenic cysts.…”

Section: Introductionmentioning

confidence: 99%

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Expression of keratin 15 in dentigerous cyst, odontogenic keratocyst and ameloblastoma

2019

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The etiology and pathogenesis of odontogenic lesions are poorly understood. Keratin 15 (K15) is a type I cytoskeletal protein that provides structural support to the cells and has been considered to be a stem cell marker. The aim of the present study was to evaluate the expression of K15 in the epithelial lining of dentigerous cysts (DCs), odontogenic keratocysts (OKCs) and ameloblastomas (ABs). The study included 41 samples of DCs (n=13), OKCs (n=12), and AB tissues (n=16). K15 protein expression was evaluated via immunohistochemistry and data were statistically analyzed using a Kruskal-Wallis test. K15 was expressed in the majority of the studied lesions with various distributions in the different study samples. The Kruskal-Wallis test revealed non-significant differences in the expression of K15 among the three odontogenic lesions (P=0.380). The present study confirmed the high expression of K15 in the different epithelial layers of DC, OKC and AB. This type of expression excludes the reliability of regarding K15 as a stem cell marker in DC, OKC and AB. However, K15 may reflect the abnormal differentiation of pathological epithelial cells in these lesions.

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Section: Discussionsupporting

confidence: 62%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Expression of keratin 15 in dentigerous cyst, odontogenic keratocyst and ameloblastoma

2019

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“…Epithelial-mesenchymal transition was found to be related to the local invasiveness of ameloblastoma, with upregulation of Slug and TGFβ and reduced E-cadherin expression (Kurioka et al 2017). COX-2 (cyclooxygenase 2) expression correlates with odontogenic epithelial proliferation in ameloblastoma, which may contribute to local invasion (Alsaegh et al 2017). CK15 and CK16 were stained positive in follicular but not plexiform ameloblastomas (Wato et al 2006).…”

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confidence: 99%

Mutational Signatures in Mandibular Ameloblastoma Correlate with Smoking

et al. 2019

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Ameloblastoma is a rare tumor of odontogenic epithelium, the low incidence rate of which precludes statistical determination of its molecular characterizations. Despite recent genomic and transcriptomic profiling, the etiology of ameloblastomas remains poorly understood. Risk factors of ameloblastoma development are also largely unknown. Whole exome sequencing was performed on 11 mandibular ameloblastoma samples. We identified 2 convergent mutational signatures in ameloblastoma: 1) a signature found in multiple types of lung cancers with probable etiology of tobacco carcinogens (COSMIC signature 4) and 2) a signature present in gingivobuccal oral squamous cell carcinoma and correlated with tobacco-chewing habits (COSMIC signature 29). These mutational signatures highlight tobacco usage or related mutagens as one possible risk factor of ameloblastoma, since the association of BRAF mutations and smoking was demonstrated in multiple studies. In addition to BRAF hotspot mutations (V600E), we observed clear inter- and intratumor heterogeneities. Interestingly, prior to BRAF mutation, important genes regulating odontogenesis mutated (e.g., corepressor BCOR), possibly playing important roles in tumorigenesis. Furthermore, recurrent mutations in the CDC73 gene, the germline mutations of which predispose patients to the development of jaw tumors, were found in 2 patients, which may lead to recurrence if not targeted by therapeutic drugs. Our unbiased profiling of coding regions of ameloblastoma genomes provides insights to the possible etiology of mandibular ameloblastoma and highlights potential disease risk factors for screening and prevention, especially for Asian patients. Because of the limited sample size and incomplete habitual, dietary, and occupational data, a causal link between tobacco usage and ameloblastoma still requires further investigations.

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“…Cyclooxygenase (Cox)-2 is a cytokine-inducible enzyme that is present in the nuclear membrane and luminal side of the endoplasmic reticulum ( 9 ). It has been reported as a pivotal factor in multiple physiological functions and pathological processes, including inflammation and tumorigenesis ( 10 ).…”

Section: Introductionmentioning

confidence: 99%

microRNA-142-3p inhibits apoptosis and inflammation induced by bleomycin through down-regulation of Cox-2 in MLE-12 cells

Guo

Lin

Ming

et al. 2017

Braz J Med Biol Res

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microRNA (miR)-142-3p is implicated in malignancy and has been identified as a biomarker for aggressive and recurrent lung adenocarcinomas. This study aimed to evaluate the inhibitory effect of miR-142-3p on apoptosis and inflammation induced by bleomycin in MLE-12 cells. MLE-12 cells were first transfected either with miR-142-3p mimic or miR-142-3p inhibitor and then the cells were exposed to 50 μg/mL of bleomycin. Thereafter, cell viability, apoptosis and the expression of pro-inflammatory cytokines were assessed using CCK-8, flow cytometry, RT-PCR and western blot analyses. Cox-2, PI3K, AKT and mTOR expressions were detected by western blotting after bleomycin was administered together with NS-398 (an inhibitor of Cox-2). As a result, cell viability was significantly decreased, as well as apoptosis and the expression of IL-1 and TNF-α were remarkably increased after 50 and 100 μg/mL of bleomycin administration. miR-142-3p overexpression alleviated bleomycin-induced apoptosis and overproduction of these two pro-inflammatory cytokines, while miR-142-3p suppression exhibited completely opposite results. Up-regulation of Cox-2 and inactivation of PI3K/AKT/mTOR were found in bleomycin-pretreated cells, while these abnormal regulations were partially abolished by miR-142-3p overexpression and NS-398. In conclusion, this study demonstrated that miR-142-3p overexpression protected bleomycin-induced injury in lung epithelial MLE-12 cells, possibly via regulating Cox-2 expression and PI3K/AKT/mTOR signaling pathway. These findings provide evidence that miR-142-3p may be a therapeutic strategy for idiopathic pulmonary fibrosis (IPF) treatment.

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Odontogenic epithelial proliferation is correlated with COX-2 expression in dentigerous cyst and ameloblastoma

Cited by 14 publications

References 52 publications

Expression of keratin 15 in dentigerous cyst, odontogenic keratocyst and ameloblastoma

Expression of keratin 15 in dentigerous cyst, odontogenic keratocyst and ameloblastoma

Mutational Signatures in Mandibular Ameloblastoma Correlate with Smoking

microRNA-142-3p inhibits apoptosis and inflammation induced by bleomycin through down-regulation of Cox-2 in MLE-12 cells

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