FGF2 Induces Breast Cancer Growth through Ligand-Independent Activation and Recruitment of ERα and PRBΔ4 Isoform to MYC Regulatory Sequences

GIULIANELLI, SEBASTIÁN; GUILLARDOY, TOMAS; RIGGIO, MARINA; PEREZ PIÑERO, CECILIA; GOROSTIAGA, MARIA ALICIA; SEQUEIRA, GONZALO; PATACCINI, GABRIELA; ABASCAL, MARIA FLORENCIA; GUERREIRO, ANA CATARINA; BARROS, ANTÓNIO; NOVARO, VIRGINIA; AMADO, FRANCISCO; ABBA, MARTIN; HELGUERO, LUISA; LANARI, CLAUDIA

Mar del Plata

Congreso; LXIII Reunión Anual de la Sociedad Argentina de Investigación Clínica (SAIC); 2018

SAIC

We have demonstrated that progesterone receptor (PR) activation is involved in fibroblast growth factor 2 (FGF2)-induced cell proliferation and tumor growth in experimental breast cancer models, and that estrogen receptor (ERα) and PR interact after progestin priming. However, it still remains unknown whether ERα and PR interact after hormone receptor ligand-independent activation. The aim of this study was to determine if ERα, in addition to PR, was also involved in FGF2-induced tumor progression and to identify interactors at hormone receptor binding sites in the MYC promoter after FGF2 stimulation. FGF2 increased ERα and PR (p