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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Cyclin D1-induced proliferation is independent of beta-catenin in Head and Neck Cancer

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Author(s):
Sales, K. U. [1] ; Giudice, F. S. [1] ; Castilho, R. M. [2] ; Salles, F. T. [3] ; Squarize, C. H. [2] ; Abrahao, A. C. [4] ; Pinto, Jr., D. S. [1]
Total Authors: 7
Affiliation:
[1] Univ Sao Paulo, Sch Dent, Dept Oral Pathol, Sao Paulo - Brazil
[2] Univ Michigan, Sch Dent, Dept Periodont & Oral Med, Ann Arbor, MI 48109 - USA
[3] Stanford Sch Med, Dept Otolaryngol Head & Neck Surg, Stanford, CA - USA
[4] Univ Fed Rio de Janeiro, Dept Oral Pathol, Rio De Janeiro - Brazil
Total Affiliations: 4
Document type: Journal article
Source: ORAL DISEASES; v. 20, n. 3, p. e42-e48, APR 2014.
Web of Science Citations: 3
Abstract

Objective Head and neck squamous cell carcinoma (HNSCC) progression and metastasis have previously been associated with the activation of phosphatidylinositol 3-kinase-protein kinase B (PI3K-Akt) and Wnt signalling pathways, which lead to the activation of pro-proliferative genes, such as cyclin D1. The current study aims to investigate whether there is a crosstalk between these pathways in HNSCC and which pathway is more likely to regulate cyclin D1. Material and Methods Two HNSCC and a control keratinocyte cell lines were treated with EGF and wortmannin to respectively activate and block the PI3K-Akt and Wnt pathways. Partial and total levels of cyclin D1, beta-catenin and Akt were evaluated by Western blotting and immunofluorescence. Twenty-four paraffin-embedded samples of human HNSCC, as well as normal oral mucosa biopsies, were also immunohistochemically evaluated for beta-catenin and cyclin D1 expression. Results Following both treatments, change in cyclin D1 protein was correlated with Akt levels only. Cytoplasmic staining for beta-catenin and loss of its membranous expression in the HNSCC invasive areas were found in 92% of the HNSCC biopsies. Conclusion Taken together, we show that the change in cyclin D1 levels is more likely to be due to the EGFR-Akt pathway activation than due to beta-catenin nuclear translocation. (AU)