WNT Signaling in Oral Cancer Initiating Cells

Menon, Reshma S.; Li, C.C.; Li, M.Z.

doi:10.1016/j.oooo.2017.06.015

Cited by 6 publications

(4 citation statements)

References 72 publications

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“…In addition, since these SNPs were associated with OC, OSCC (Andrade Filho et al., 2011; de Freitas et al., 2019), and also to OPMD, it could be suggested that variations in Wnt genes that were shown to be involved with OC may also increase the susceptibility of developing OPMD or OSCC. They are three different phenotypes that share similar variations in Wnt genes, which are involved in cell proliferation and differentiation (Andrade Filho et al., 2011; Chiquet et al., 2008; de Freitas et al., 2019; Ejaz & Ghafoor, 2019; Menon, 2017; Zhan et al., 2017).…”

Section: Discussionmentioning

confidence: 99%

Polymorphisms associated with oral clefts as potential markers for oral pre and malignant disorders

da Silva,

Freitas,

Vieira

2023

Oral Diseases

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ObjectiveTo investigate whether genes in the Wnt pathway, which have been previously associated with both oral clefts and oral squamous cell carcinoma, are also associated with oral potentially malignant disorders (leukoplakia, erythroplakia and lichen planus).Materials and MethodsCase–control study: Dataset consisted of clinical information linked to DNA samples from affected subjects diagnosed with oral potential malignant disorders and oral cancer and their matched controls. Individual samples, clinical history, and potential risk factors were obtained through the Dental Registry and DNA Repository project of the School of Dental Medicine, University of Pittsburgh. The rs1533767 (WNT11), rs9879992 (GSK3B), and rs3923087 (AXIN2) were tested. After genomic DNA had been extracted, genotyping was performed blindly to clinical diagnosis status. Representation of genotypes and alleles in affected subjects in comparison to the unaffected individuals was determined using PLINK. Additional analysis was performed to investigate associations between environmental (socioeconomic/lifestyle) risk factors and the oral pathologies studied using STATA.ResultsTwo of the SNPs tested (rs9879992 in GSK3B and rs3923087 in AXIN2) were statistically, significantly associated with the pathologies studied (p = 0.039 and 0.038, respectively).ConclusionSingle‐nucleotide polymorphisms in genes in the Wnt pathway were associated with oral potentially malignant disorders.

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Section: Discussionmentioning

confidence: 99%

Polymorphisms associated with oral clefts as potential markers for oral pre and malignant disorders

da Silva,

Freitas,

Vieira

2023

Oral Diseases

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“…The Wnt signaling pathway is implicated in OSCC, and its abnormal activation, often through mutations or dysregulation of its components, such as β-catenin, is observed in OSCC. This dysregulation leads to uncontrolled cell growth, invasion, and metastasis in OSCC [257]. Additionally, epigenetic modifications, like hypermethylation of the SOX17 gene promoter, can further contribute to the abnormal activation of the Wnt pathway in OSCC [258].…”

Section: Tfpi2 Sox17 and Gata4mentioning

confidence: 99%

Epigenetic Regulation in Oral Squamous Cell Carcinoma Microenvironment: A Comprehensive Review

Mesgari,

Esmaelian,

Nasiri

et al. 2023

Cancers

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Oral squamous cell carcinoma (OSCC) is a prevalent and significant type of oral cancer that has far-reaching health implications worldwide. Epigenetics, a field focused on studying heritable changes in gene expression without modifying DNA sequence, plays a pivotal role in OSCC. Epigenetic changes, encompassing DNA methylation, histone modifications, and miRNAs, exert control over gene activity and cellular characteristics. In OSCC, aberrant DNA methylation of tumor suppressor genes (TSG) leads to their inactivation, subsequently facilitating tumor growth. As a result, distinct patterns of gene methylation hold promise as valuable biomarkers for the detection of OSCC. Oral cancer treatment typically involves surgery, radiation therapy, and chemotherapy, but even with these treatments, cancer cells cannot be effectively targeted and destroyed. Researchers are therefore exploring new methods to target and eliminate cancer cells. One promising approach is the use of epigenetic modifiers, such as DNA methyltransferase (DNMT) inhibitors and histone deacetylase (HDAC) inhibitors, which have been shown to modify abnormal epigenetic patterns in OSCC cells, leading to the reactivation of TSGs and the suppression of oncogenes. As a result, epigenetic-targeted therapies have the potential to directly alter gene expression and minimize side effects. Several studies have explored the efficacy of such therapies in the treatment of OSCC. Although studies have investigated the efficacy of epigenetic therapies, challenges in identifying reliable biomarkers and developing effective combination treatments are acknowledged. Of note, epigenetic mechanisms play a significant role in drug resistance in OSCC and other cancers. Aberrant DNA methylation can silence tumor suppressor genes, while alterations in histone modifications and chromatin remodeling affect gene expression related to drug metabolism and cell survival. Thus, understanding and targeting these epigenetic processes offer potential strategies to overcome drug resistance and improve the efficacy of cancer treatments in OSCC. This comprehensive review focuses on the complex interplay between epigenetic alterations and OSCC cells. This will involve a deep dive into the mechanisms underlying epigenetic modifications and their impact on OSCC, including its initiation, progression, and metastasis. Furthermore, this review will present the role of epigenetics in the treatment and diagnosis of OSCC.

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“…Immunohistochemical studies revealed co-expression of βcatenin and LEF1 in OSCC, suggesting activation of Wnt/ 2 -catenin signaling. Increased Axin2 fluorescence was visualized in basal cells in OSCC, thus being able to confirm that Wnt-responsive CICs in OSCC contribute its malignant progression [ 109 ].…”

Section: Signaling Pathways In Emtmentioning

confidence: 99%

Signaling pathways promoting epithelial mesenchymal transition in oral submucous fibrosis and oral squamous cell carcinoma

Shetty

Sharma²,

Fonseca

et al. 2020

Japanese Dental Science Review

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Summary Epithelial-mesenchymal transition (EMT) is a critical process that occurs during the embryonic development, wound healing, organ fibrosis and the onset of malignancy. Emerging evidence suggests that the EMT is involved in the invasion and metastasis of cancers. The inflammatory reaction antecedent to fibrosis in the onset of oral submucous fibrosis (OSF) and the role of EMT in its malignant transformation indicates a hitherto unexplored involvement of EMT. This review focuses on the role of EMT markers which are regulators of the EMT mediated complex network of molecular mechanisms involved in the pathogenesis of OSF and OSCC. Further the gene enrichment analysis and pathway analysis supports the association of the upregulated and downregulated genes in various EMT regulating pathways.

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WNT Signaling in Oral Cancer Initiating Cells

Cited by 6 publications

References 72 publications

Polymorphisms associated with oral clefts as potential markers for oral pre and malignant disorders

Polymorphisms associated with oral clefts as potential markers for oral pre and malignant disorders

Epigenetic Regulation in Oral Squamous Cell Carcinoma Microenvironment: A Comprehensive Review

Signaling pathways promoting epithelial mesenchymal transition in oral submucous fibrosis and oral squamous cell carcinoma

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