β-catenin expression in areca quid chewing-associated oral squamous cell carcinomas and upregulated by arecoline in human oral epithelial cells

Lee, Shiuan Shinn; Tsai, Chien‐Hsiung; Tsai, Lo Lin; Chou, Ming Chih; Chang, Yi-Chun

doi:10.1016/j.jfma.2010.11.002

Cited by 19 publications

(13 citation statements)

References 35 publications

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“…In vitro studies have demonstrated that ANE treatment induced the phosphorylation of GSK-3 β [34–36]. β -catenin expression was increased by arecoline in a dose-dependent manner [37]. The results of this study suggest that ANE treatment may facilitate OPC differentiation and myelination processes and that the AMPK signaling pathway may be involved in this process.…”

Section: Discussionmentioning

confidence: 63%

The Protective Effects ofAreca catechuExtract on Cognition and Social Interaction Deficits in a Cuprizone-Induced Demyelination Model

Adilijiang

Guan

et al. 2015

Evidence-Based Complementary and Alternative Medicine

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Schizophrenia is a serious psychiatric illness with an unclear cause. One theory is that demyelination of white matter is one of the main pathological factors involved in the development of schizophrenia. The current study evaluated the protective effects of Areca catechu nut extract (ANE) on a cuprizone-induced demyelination mouse model. Two doses of ANE (1% and 2%) were administered orally in the diet for 8 weeks. Animals subjected to demyelination showed impaired spatial memory and less social activity. In addition, mice subjected to demyelination displayed significant myelin damage in cortex and demonstrated a higher expression of NG2 and PDGFRα and AMPK activation. ANE treatment not only significantly enhanced cognitive ability and social activity, but also protected myelin against cuprizone toxicity by promoting oligodendrocyte precursor cell (OPC) differentiation. In addition, ANE treatment demonstrated significant dephosphorylation of AMPKα, indicating a regulatory role for ANE in schizophrenia. This study showed that ANE treatment may enhance cognitive ability and social activity by facilitating OPC differentiation and protecting against myelin damage in cortex. Results also suggest the AMPK signaling pathway may be involved in this process.

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Section: Discussionmentioning

confidence: 63%

The Protective Effects ofAreca catechuExtract on Cognition and Social Interaction Deficits in a Cuprizone-Induced Demyelination Model

Adilijiang

Guan

et al. 2015

Evidence-Based Complementary and Alternative Medicine

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“…Abnormal expression of cyclin D1 was shown in various types of malignancies, including oral carcinoma (Lee et al, 2012). Cyclin D1 expression was associated with the tumor staging, lymphnode metastasis, grading and tumor size/thickness (Sarkar et al, 2015).…”

Section: Discussionmentioning

confidence: 99%

Emodin Downregulates Cell Proliferation Markers During Dmba Induced Oral Carcinogenesis in Golden Syrian Hamsters

Manimaran¹,

Buddhan²,

Manoharan³

2017

Afr J Tradit Complement Altern Med

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Background: Cell-cycle disruption is the major characteristic features of neoplastic transformation and the status of cell-cycle regulators can thus be utilized to assess the prognostic significance in patients with cancer. The PCNA, cyclin D1, CDK4, CDK6 and survivin expression in the buccal mucosa was utilized to evaluate the Emodin efficacy on abnormal cell proliferation during 7,12-dimethylbenz(a)anthracene (DMBA) induced oral carcinogenesis in golden Syrian hamsters. Materials and methods: Topical application of DMBA, three times a week for 14 weeks, on the hamsters' buccal pouches developed well differentiated squamous cell carcinoma. Results: Cyclin D1 and PCNA over-expression and up-regulation of CDK4, CDK6 and survivin were noticed in the buccal mucosa of hamsters treated with DMBA alone. Emodin administration (50mg/kg b.w) orally to hamsters treated with DMBA down-regulated the expression of cell proliferation markers in the buccal mucosa. Conclusions:The anti-cell proliferative role of Emodin is owing to its modulating efficacy on cell-cycle markers towards the tumor suppression during DMBA induced oral carcinogenesis.

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“…Arecoline-induced β-catenin overexpression in oral epithelial cells was reduced by ERK and PI3K small molecule inhibitors [33]. It has been observed that the overexpression of TWIST1 transcription factor increased β-catenin-dependent transcription of c-MYC and MMP-2, which resulted in increased cell invasion.…”

Section: Functional Significance Of Wnt/β-catenin Pathway Dysregulationmentioning

confidence: 99%

“…Indeed, many immunohistochemical analyses have documented the membranous localization of β-catenin in cells of normal mucosal epithelium [24,25], while cytoplasmic or nuclear presence of β-catenin, which can mark canonical Wnt pathway activation, is infrequent in normal epithelial cells [26,27]. In contrast, dysplastic or cancerous epithelium shows a decrease in membranous β-catenin level and abnormal delocalization of β-catenin to cytoplasmic and, sometimes, also nuclear compartments [13,18,24,[26][27][28][29][30][31][32][33]. A progressive loss of membranous β-catenin was reported during transition from hyperplasia to dysplasia and carcinoma [34].…”

Section: Introductionmentioning

confidence: 99%

The Significance of the Dysregulation of Canonical Wnt Signaling in Head and Neck Squamous Cell Carcinomas

Paluszczak

2020

Cells

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The knowledge about the molecular alterations which are found in head and neck squamous cell carcinomas (HNSCC) has much increased in recent years. However, we are still awaiting the translation of this knowledge to new diagnostic and therapeutic options. Among the many molecular changes that are detected in head and neck cancer, the abnormalities in several signaling pathways, which regulate cell proliferation, cell death and stemness, seem to be especially promising with regard to the development of targeted therapies. Canonical Wnt signaling is a pathway engaged in the formation of head and neck tissues, however it is not active in adult somatic mucosal cells. The aim of this review paper is to bring together significant data related to the current knowledge on the mechanisms and functional significance of the dysregulation of the Wnt/β-catenin pathway in head and neck tumors. Research evidence related to the role of Wnt signaling activation in the stimulation of cell proliferation, migration and inhibition of apoptosis in HNSCC is presented. Moreover, its role in promoting stemness traits in head and neck cancer stem-like cells is described. Evidence corroborating the hypothesis that the Wnt signaling pathway is a very promising target of novel therapeutic interventions in HNSCC is also discussed.Cells 2020, 9, 723 2 of 20 blocking the interaction between PD-1 receptor and PD-L1, may be beneficial in patients with advanced, metastatic or recurrent HNSCC [7]. However, other therapeutic options are also necessary for the better clinical management of HNSCC patients. To that end, molecular alterations observed in HNSCC need to be studied in detail, in order to point to promising drug targets. Mechanisms of Wnt/β-Catenin Pathway Activation in HNSCCRecent genomic analyses have shown the prevalence of genetic driver alterations in HNSCC, which most frequently affect genes associated with receptor tyrosine kinase (e.g., EGFR, MET, KIT), PI3K, p53, Notch or Hippo signaling pathways. On the other hand, genetic alterations in genes related to canonical Wnt signaling were rarely detected in HNSCC [8,9]. In contrast to colorectal cancers, which show molecular alterations driving Wnt signaling activation in around 90% of cases [9], HNSCC were shown to lack CTNNB1 mutations and APC mutations were present infrequently [10][11][12][13][14][15][16]. The mutations of FAT1 tumor suppressor, which encodes a protocadherin protein that binds and inactivates β-catenin, were detected in some cases of HNSCC [17]. However, the activation of the Wnt/β-catenin pathway in HNSCC seems to be more prevalent than it is suggested by genetic findings, due to cross-talk with other molecular alterations, which can lead to pathway cross-activation. Indeed, it has been shown that β-catenin can be activated via enhanced EGFR or PI3K signaling, which belong to the most frequently dysregulated signaling pathways in HNSCC. In this regard, elevated EGFR expression was associated with delocalized β-catenin expression [13]. In another study, the nuclear ...

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β-catenin expression in areca quid chewing-associated oral squamous cell carcinomas and upregulated by arecoline in human oral epithelial cells

Cited by 19 publications

References 35 publications

The Protective Effects ofAreca catechuExtract on Cognition and Social Interaction Deficits in a Cuprizone-Induced Demyelination Model

The Protective Effects ofAreca catechuExtract on Cognition and Social Interaction Deficits in a Cuprizone-Induced Demyelination Model

Emodin Downregulates Cell Proliferation Markers During Dmba Induced Oral Carcinogenesis in Golden Syrian Hamsters

The Significance of the Dysregulation of Canonical Wnt Signaling in Head and Neck Squamous Cell Carcinomas

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