ChIP-seq of estrogen receptor a in wild type MCF7-V and in MCF7-V breast carcinoma cell line transduced with a doxycyline-inducible construct to express ZEB1.

The epithelial to mesenchymal transition (EMT) is implicated in the metastatic spread of breast cancer cells. EMT transcription factors (TF) regulate different stages of EMT states. In breast cancers, estrogen receptor a (ERa) maintains the epithelial characteristics of breast tumors and is indispensable for efficient endocrine therapy. In this study we investigate whether and how ZEB1, an EMT-TF affects ERa signaling at early stages of EMT and metastasis. We did ERa ChIP-seq in wild type MCF7-V cells for comparative studies. We also did ERa ChIP-seq in cells stably expressing a doxycycline-inducible construct to express ZEB1. This was to determine the impact of ZEB1 on the ERa cistrome in MCF7-V breast cancer cells induced with DMSO, 17-beta estradiol (E2), and forskolin + 3-isobutyl-1-methylxanthine (IBMX) (FI). Overall design: We did ChIP-seq in wild type MCF7-V breast cancer cells and in cells stably expressing a doxycyline-inducible construct to express ZEB1 in presence of dxycycline. To induce ZEB1 in stable cell line we used 2 µg/ml doxycyline (DOX).