Fig. 4.

Endocrine treatment induces transcriptional regulation of S100β which is disrupted by tyrosine kinase inhibition. a Expression of ERα, PR, p-Src, c-Src, HOXC11, SRC-1, S100β, and β-actin in a panel of endocrine resistant (LY2, LetR) and sensitive (MCF-7, ARO) cell lines (representative blots from n = 3). b Chromatin immunoprecipitation of SRC-1 and HOXC11 of the S100β promoter region in LY2 cells treated with tamoxifen alone or in combination with dasatinib inhibits SRC-1 and HOXC11 recruitment to the S100β promoter (graphs are representative of the mean relative recruitment values relative to tamoxifen-treated controls, n = 3 ± SEM, p ≤ 0.05). c Inhibition of S100β protein expression with tyrosine kinase inhibitors PP2 or dasatinib in the endocrine resistant LY2 cells treated with tamoxifen (representative blots from n = 3). d Schematic representation of S100β pathway, showing long-term exposure to endocrine therapy induces expression of S100β in an Src-dependent manner