Skip to main content
Fig. 4 | Breast Cancer Research

Fig. 4

From: SHP2 acts both upstream and downstream of multiple receptor tyrosine kinases to promote basal-like and triple-negative breast cancer

Fig. 4

Analysis of epidermal growth factor receptor (EGFR) and Src homology phosphotyrosyl phosphatase 2 (SHP2) expression in basal-like and triple-negative breast cancer (BTBC) tumors and cell lines. a Representative 3+ immunohistochemistry (IHC) pictures of SHP2 and EGFR expression in tumor and adjacent normal tissue. b Immunofluorescence costaining for SHP2 and EGFR showing state of expression in normal-looking, hyperplastic, ductal carcinoma in situ (DCIS), and infiltrating ductal carcinoma (IDC) regions of a representative specimen. Note that the level of expression for both proteins is comparable in various stages of tumor development. c Analysis of SHP2 and EGFR co-overexpression in breast cancer cell lines and in experimentally produced EGFR-overexpressing cells. The BT-474 breast cancer cell line that overexpresses human epidermal growth factor receptor 2 (HER2), MCF-10A, and mouse embryonic fibroblasts (MEFs) ectopically overexpressing HER2 and/or EGFR was also used in this analysis. Parental human mammary luminal epithelial cells (HMLE), MCF-10A cells, and MEFs were used as negative controls for receptor tyrosine kinase overexpression. d EGFR and SHP2 band density measurements from at least three independent experiments analyzed as shown in (c). The EGFR (open bar) and SHP2 (hatched bar) band densities in the various lanes were adjusted using β-actin band densities. DAPI 4′,6-diamidino-2-phenylindole

Back to article page