FGF2 Induces Breast Cancer Growth through Ligand-Independent Activation and Recruitment of ERα and PRBΔ4 Isoform to MYC Regulatory Sequences. Giulianelli S, Riggio M, Guillardoy T, Pérez Piñero C

GUILLARDOY TOMÁS; SEQUEIRA GONZALO; TOLEDO MARIA FERNANDA; BARROS ANTONIO; AMADO FRANCISCO; HELGUERO LUISA A; RIGGIO MARINA; GOROSTIAGA MARÍA ALICIA; ABASCAL MARIA FLORENCIA; GUERREIRO ANA C; MONTEIRO FATIMA L; ABBA MARTIN; GIULIANELLI SEBASTIÁN; PÉREZ CECILIA; PATACCINI GABRIELA; JACOBSEN BRITTA M; NOVARO VIRGINIA; GASS HUGO; LANARI CLAUDIA

Mar del Plata

Congreso; Sociedad Argentina de Investigacion Clinica (SAIC); 2018

We have previously demonstrated that a) progesterone receptor (PR) activation is involved in fibroblast growth factor 2 (FGF2)-induced cell proliferation and tumor growth in experimental breast cancer models and b) that estrogen receptors (ERα) and PR interact after progestin priming. However, it still remains unknown whether ER and PR interact after their 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 determine partners at the hormone receptor binding sites of the MYC enhancer and proximal promoters after FGF-2 priming.FGF2 increased phospho (p)-ERα and p-PR (p