Expression of molecules related to <scp>AKT</scp> pathway as putative regulators of ameloblastoma local invasiveness

Cecim, Rodolpho L.; Carmo, Hicso A. F.; Kataoka, Maria S. S.; Freitas, Vanessa M.; Júnior, Sérgio de Melo Alves; Pedreira, Erick Nelo; Jaeger, Ruy Gastaldoni; Pinheiro, João de Jesus Viana

doi:10.1111/jop.12103

Cited by 12 publications

(22 citation statements)

References 27 publications

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“…It was reported that 93% of KCOT expressed phospho-Thr308 Akt, 40% expressed phospho-Thr308 Akt, 83% expressed phospho-RPS6, and 30% expressed all three (n=30). Two additional studies reported that 100% of ameloblastomas expressed phosphorylated Akt, but these reports did not indicate which phosphorylation site(s) were examined [67, 82]. However, one study clarified that while all ameloblastomas tested also expressed PTEN, the expression was at a lower level compared to that in normal tooth germ, indicating that there may be increased Akt activity in ameloblastomas (Kumamoto 2007).…”

Section: Aktmentioning

confidence: 99%

Molecular Signaling in Benign Odontogenic Neoplasia Pathogenesis

Amm

MacDougall

2016

Curr Oral Health Rep

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Several molecular pathways have been shown to play critical roles in the pathogenesis of odontogenic tumors. These neoplasms arise from the epithelial or mesenchymal cells of the dental apparatus in the jaw or oral mucosa. Next generation genomic sequencing has identified gene mutations or single nucleotide polymorphisms associated with many of these tumors. In this review, we focus on two of the most common odontogenic tumor subtypes: ameloblastoma and keratocystic odontogenic tumors. We highlight gene expression and protein immunohistological findings and known genetic alterations in the hedgehog, BRAF/Ras/MAPK, epidermal growth factor receptor, Wnt and Akt signaling pathways relevant to these tumors. These various pathways are explored to potentially target odontogenic tumors cells and prevent growth and recurrence of disease. Through an understanding of these signaling pathways and their crosstalk, molecular diagnostics may emerge as well as the ability to exploit identified molecular differences to develop novel molecular therapeutics for the treatment of odontogenic tumors.

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Section: Aktmentioning

confidence: 99%

Molecular Signaling in Benign Odontogenic Neoplasia Pathogenesis

Amm

MacDougall

2016

Curr Oral Health Rep

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“…27 The rate of cell proliferation may lead to local invasiveness of AB. 28 Therefore, lncRNA ENST00000512916 could regulate AB cell proliferation and apoptosis. Identification of proliferative activity in tumors can be used to predict their biological behavior.…”

Section: Discussionmentioning

confidence: 99%

<p>A Novel lncRNA ENST00000512916 Facilitates Cell Proliferation, Migration and Cell Cycle Progression in Ameloblastoma</p>

Sun¹,

Niu²,

Wang³

et al. 2020

OTT

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Our purpose was to identify up-regulated long noncoding RNA ENST00000512916 in ameloblastoma (AB) and explore its role in the progression of AB. Methods: We analyzed lncRNA microarray expression profile between six paired AB and normal oral mucosa (NOM) tissues. An up-regulated lncRNA, ENST00000512916 was identified and validated by real-time qPCR. Cell proliferation, migration and cell cycle were detected by CCK-8 assay, transwell chamber and flow cytometry, respectively. Western blotting analysis was used to measure the expression of cell-cycle-related proteins including CyclinD1 and Cyclin-dependent kinase (CDK) 2/4/6. In addition, Xenograft tumor model was constructed to investigate tumor growth. Results: Real-time qPCR confirmed that lncRNA ENST00000512916 was up-regulated in AB tissues. ENST00000512916 knockdown significantly inhibited cell proliferation, migration and the expression of CDK2/4/6 in AM-1 cells. Moreover, ENST00000512916 knockdown suppressed tumor growth in vivo. We also found that ENST00000512916 overexpression significantly promoted the expression of HOXC13 in AM-1 cells. Overexpression of ENST00000512916 promoted cell cycle progression in AM-1 cells, which was reversed by HOXC13 knockdown. Conclusion: Our findings reveal that lncRNA ENST00000512916 promotes cell proliferation, migration and cell cycle progression of AB.

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“…Moreover, β-catenin upregulation leads to increase in COX2 and finally MMP 9 which plays a critical role in angiogenesis and invasion. [ 60 ] Wei et al . in 2013 analyzed 30 Ameloblastomas and 10 normal mucosa for the presence of β-catenin and Axin2 using RT-PCR, Western Blot Analysis and IHC.…”

Section: β-Catenin In Odontogenic Cysts and Tumorsmentioning

confidence: 99%

Beta-catenin in disease

Prakash

Swaminathan

Nagamalini

et al. 2016

J Oral Maxillofac Pathol

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In continuation with the previous review on “β-catenin in health”, in this review we discuss the role of β-catenin in the pathogenesis of common oral lesions in the oral and maxillofacial region- oral potentially malignant disorders, their progression to oral squamous cell carcinoma, salivary gland tumors and odontogenic tumours. This review is based on a pubmed search of all the lesions included in the review.

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Expression of molecules related to AKT pathway as putative regulators of ameloblastoma local invasiveness

Abstract: Results suggest that proteins studied are present and probably involved in a functional pathway in neoplastic cells and stroma and may therefore influence the local invasiveness of ameloblastoma.

Cited by 12 publications

References 27 publications

Molecular Signaling in Benign Odontogenic Neoplasia Pathogenesis

Molecular Signaling in Benign Odontogenic Neoplasia Pathogenesis

<p>A Novel lncRNA ENST00000512916 Facilitates Cell Proliferation, Migration and Cell Cycle Progression in Ameloblastoma</p>

Beta-catenin in disease

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