| Autor: |
Sales, KU, Giudice, FS, Castilho, RM, Salles, FT, Squarize, CH, Abrahao, AC, Pinto, DS |
| Předmět: |
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| Zdroj: |
Oral Diseases; Apr2014, Vol. 20 Issue 3, pe42-e48, 7p, 2 Color Photographs, 1 Black and White Photograph, 1 Chart |
| Abstrakt: |
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 ( PI3 K- 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 PI3 K- 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. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
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