scholarly journals Epidermal growth factor receptor variant III mediates head and neck cancer cell invasion via STAT3 activation

Oncogene ◽  
2010 ◽  
Vol 29 (37) ◽  
pp. 5135-5145 ◽  
Author(s):  
S E Wheeler ◽  
S Suzuki ◽  
S M Thomas ◽  
M Sen ◽  
R J Leeman-Neill ◽  
...  
Keyword(s):  
Epidermal Growth Factor Receptor ◽  
Head And Neck Cancer ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Head And Neck ◽  
Cancer Cell ◽  
Cell Invasion ◽  
Growth Factor Receptor ◽  
Cancer Cell Invasion ◽  
Epidermal Growth

Epidermal growth factor receptor gene amplification and expression in head and neck cancer cell lines

Head & Neck ◽  
1989 ◽  
Vol 11 (5) ◽  
pp. 437-442 ◽  
Author(s):  
Ralph R. Weichselbaum ◽  
Edward J. Dunphy ◽  
Michael A. Beckett ◽  
Allen G. Tybor ◽  
William J. Moran ◽  
...  
Keyword(s):  
Epidermal Growth Factor Receptor ◽  
Head And Neck Cancer ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Head And Neck ◽  
Cell Lines ◽  
Cancer Cell ◽  
Receptor Gene ◽  
Growth Factor Receptor ◽  
Epidermal Growth

scholarly journals Differentiated thyroid cancer cell invasion is regulated through epidermal growth factor receptor-dependent activation of matrix metalloproteinase (MMP)-2/gelatinase A

2006 ◽  
Vol 13 (4) ◽  
pp. 1173-1183 ◽  
Author(s):  
Michael W Yeh ◽  
Jean-Philippe Rougier ◽  
Jin-Woo Park ◽  
Quan-Yang Duh ◽  
Mariwil Wong ◽  
...  
Keyword(s):  
Epidermal Growth Factor Receptor ◽  
Thyroid Cancer ◽  
Growth Factor ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cell Invasion ◽  
Growth Factor Receptor ◽  
Thyroid Cancer Cell ◽  
Cancer Cell Invasion ◽  
Epidermal Growth

Mechanisms of invasion in thyroid cancer remain poorly understood. We hypothesized that signaling via the epidermal growth factor receptor (EGFR) stimulates thyroid cancer cell invasion by altering the expression and cleavage of matrix metalloproteinases (MMPs). Papillary and follicular carcinoma cell lines were treated with EGF, the EGFR tyrosine kinase inhibitor AG1478, and the MMP inhibitors GM-6001 and Col-3. Flow cytometry was used to detect EGFR. In vitro invasion assays, gelatin zymography, and quantitative reverse transcription-PCR were used to assess the changes in invasive behavior and MMP expression and activation. All cell lines were found to overexpress functional EGFR. EGF stimulated invasion by thyroid cancer cells up to sevenfold (P < 0.0001), a process that was antagonized completely by AG1478 and Col-3, partially by GM-6001, but not by the serine protease inhibitor aprotinin. EGF upregulated expression of MMP-9 (2.64- to 8.89-fold, P < 0.0001) and membrane type-1 MMP (MT1-MMP, 1.97- to 2.67-fold, P < 0.0001). This effect was blocked completely by AG1478 and partially by Col-3. The activation of MMP-2 paralleled MT1-MMP expression. We demonstrate that MMPs are critical effectors of invasion in the papillary and follicular thyroid cancer cell lines studied. Invasion is regulated by signaling through EGFR, an effect mediated by augmentation of gelatinase expression and activation. MMP inhibitors and growth factor antagonists may be effective tumoristatic agents for the treatment of aggressive thyroid carcinomas.

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