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Inhibition of SRC with AZD0530 reveals the Src-focal adhesion kinase complex as a novel therapeutic target in papillary and anaplastic thyroid cancers
Journal of Clinical Endocrinology and Metabolism, 03/26/09

Schweppe RE et al. - In a trial to determine the role of Src and focal adhesion kinase (FAK) in growth and invasion of papillary and anaplastic thyroid cancer (PTC and ATC), it was found that inhibition of the Src-FAK complex represents a promising therapeutic strategy for pts with advanced thyroid cancer and phospho-FAK represents a potential biomarker for response.

Methods

PTC and ATC cells were treated with the oral Src inhibitor, AZD0530, to determine the consequences of Src inhibition using growth and invasion assays.
FAK and phospho-FAK levels were analyzed in cell lines as well as in PTC tumor samples.

Results

AZD0530 treatment inhibited growth and invasion of 4 of 5 thyroid cancer cell lines and inhibition did not correlate with basal levels of phospho-Src.
FAK is phosphorylated at tyrosine residue 861 (pY861) in PTC and ATC cells and high levels of phospho-FAK correlate with AZD0530 sensitivity.
pY861-FAK phosphorylation is Src-dependent.
Sensitivity to AZD0530 was confirmed using a preclinical 3D-culture model.
Phospho-ERK1/2 was not affected by AZD0530, indicating Src signaling does not require MAPK.
FAK and pY861-FAK were expressed in 10/10 and 5/10 PTC tumors, respectively.

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