DEVELOPMENT OF A HORMONE INDEPENDENT AND TAMOXIFEN RESISTANT BREAST CANCER CELL MODEL BY RAC1 UPREGULATION ACTIVITY

NAZARENO GONZÁLEZ; GEORGINA A. CARDAMA; DANIEL F. ALONSO; DANIEL E. GOMEZ; PABLO LORENZANO MENNA

Bariloche

Simposio; The Third South American Symposium in Signal Transduction and Molecular Medicine? (SISTAM 2015); 2015

Additionally to chemotherapeutic treatment, ERα-positive breast cancer patients receive anti-hormonal agents such as Tamoxifen (Tam) and aromatase inhibitors. Unfortunately, a significant proportion of patients who receive adjuvant endocrine treatment still develop recurrence. There is a large amount of evidence that involves Rac1 GTPase in the transition from hormone-dependent to hormone-independent growth, which influences the loss of sensitivity to hormone treatments. The main goal of this work was to develop a hormone-independent breast cancer model, based on the upregulation of Rac1 activity. This cell model would allow us to test the role of Rac1 protein in several mechanisms of acquired endocrine resistance. The MCF7::C1199 model was established by transfecting the hormone-dependent MCF7 cells with a constitutively active form of the GEF activator Tiam1. This model showed high levels of active Rac1, a significant increase in cell migration (p