Estrogen-dependent and estrogen-independent mechanisms contribute to AIB1-mediated tumor formation.

ABSTRACT: We have previously reported the oncogenic properties of the gene amplified in breast cancer 1 (AIB1), a member of the p160 family of hormone receptor coactivators. In a transgenic mouse model, AIB1 overexpression resulted in a high incidence of tumors in various tissues, including mammary gland, uterus, lung, and pituitary. To determine whether the AIB1 oncogenicity in this model depended on its function as an estrogen receptor (ER) coactivator, we abolished ER signaling through two independent approaches, by performing ovariectomy on AIB1 transgenic (AIB1-tg) mice to prevent gonadal estrogen production and by crossing AIB1-tg mice with ERalpha-null mutant mice. Ovariectomized (ovx) mice, but not AIB1 x ERalpha-/- mice, still developed mammary gland hyperplasia and ductal carcinoma in situ

SUBMITTER: Torres-Arzayus MI 

PROVIDER: S-EPMC2879596 | biostudies-literature | 2010 May

REPOSITORIES: biostudies-literature