TNK2 preserves epidermal growth factor receptor expression on the cell surface and enhances migration and invasion of human breast cancer cells-1

NK2 are shown relative to β-actin protein levels in the following cell lines: HB2, normal human breast epithelial cells; MCF-7, MDA-MB-468, and T47D human breast cancer cells; HC11 murine mammary epithelial cells; and human breast cancer cell line, MDA-MB-231. TNK2 is recruited to the EGFR following activation of the receptor in MDA-MB-231 cells, as indicated by coimmunoprecipitation in the presence and absence of epidermal growth factor (EGF) stimulation at 100 ng/ml. The association of EGFR and TNK2 in MDA-MB-231 cells is not dependent on the phosphorylation status of TNK2, as indicated by the ability of wildtype (Wt), mutant kinase-deficient (Kd) and constitutively active (Ca) TNK2 to immunoprecipitate activated EGFR. The percentage cell surface expression of EGFR is shown in serum-starved MDA-MB-231 cells treated with EGF (100 ng/ml) for the indicated times. Reduced numbers of basal cell surface EGFRs are seen in cells treated with targeting SiRNA (S1) relative to the nontargeting SiRNA control (N), as measured by a fluorescein isothiocyanate-conjugated anti-EGFR antibody by fluorescence-activated cell sorting analysis. On average, a 27% reduction of cell surface receptors can be seen at timepoint 0 (= 0.0135). A representative western blot illustrating the downregulation of TNK2 achieved by SiRNA treatment relative to β-actin is shown.<p><b>Copyright information:</b></p><p>Taken from "TNK2 preserves epidermal growth factor receptor expression on the cell surface and enhances migration and invasion of human breast cancer cells"</p><p>http://breast-cancer-research.com/content/10/2/R36</p><p>Breast Cancer Research : BCR 2008;10(2):R36-R36.</p><p>Published online 24 Apr 2008</p><p>PMCID:PMC2397538.</p><p>