The role of AIB1 in breast cancer

Abstract

Abstract. Amplified in breast cancer 1 (AIB1) is a member of the p160 steroid receptor coactivator family that mediates the transcriptional activities of nuclear receptors including estrogen receptor (ER) and progesterone receptor (PR), as well as certain other transcription factors, including E2F1 and p53. AIB1 is widely implicated in nuclear receptor-mediated diseases, particularly malignant diseases, including breast, prostate, gastric and pancreatic cancers. AIB1 was initially implicated in hormone-dependent breast cancer, where increasing levels of AIB1 mRNA and protein were detected in some of these specimens and the overexpression of AIB1 in mice led to an increased incidence of tumors. More recent studies revealed that AIB1 also affects the growth of hormone-independent breast cancer via signaling pathways such as those of E2F1, IGF-I, EGF and PI3K/Akt/ mTOR. The pleiotropic effect of AIB1 and the roles it plays in both normal development and cancer have presented a great challenge to formulating an effective therapeutic strategy for breast cancer. In this review, we highlight the significant progress made with the recent findings and present an overview of the current understanding of the influence of AIB1 on breast cancer via hormone-dependent and -independent signaling pathways.

Chromatin reprogramming as an adaptation mechanism in advanced prostate cancer

“…Interestingly, we showed that a number of the AR coregulators were AR regulated and that enhanced expression of a subset of these coregulators was observed in castration-challenged PC cells ectopically overexpressing AR (Urbanucci et al 2008). Among the androgen-regulated coregulators identified were amplified in breast cancer 1 (AIB1) and CBP, both HATs which have been shown to increase nuclear receptors' activities and are implicated in mechanisms of drug resistance (Chang & Wu 2012, Culig 2016, Jin et al 2017.…”

Relation among Aromatase P450 and Tumoral Growth in Human Prolactinomas

“…Likewise, PTTG stimulates fibroblast growth factor 2 (FGF2) and vascular endothelial growth factor (VEGF) production, accelerates tissue angiogenesis, and facilitates pituitary tumor progression through local invasion of the surrounding tissues [ 99 , 102 ]. On the other hand, AIB1, an important factor in the development of breast cancer [ 103 ], is overexpressed by the action of 17-β-estradiol [ 104 ], and AIB1 may be an important diagnostic and therapeutic target in breast cancer [ 105 ]. The relation between ERα and AIB1 is well established [ 103 , 106 , 107 ], and the over-expression of AIB1 could be related to the increases in the incidence of pituitary tumors in mice [ 108 ].…”

“…On the other hand, AIB1, an important factor in the development of breast cancer [ 103 ], is overexpressed by the action of 17-β-estradiol [ 104 ], and AIB1 may be an important diagnostic and therapeutic target in breast cancer [ 105 ]. The relation between ERα and AIB1 is well established [ 103 , 106 , 107 ], and the over-expression of AIB1 could be related to the increases in the incidence of pituitary tumors in mice [ 108 ].…”

Steroid receptor coactivator-3 is a pivotal target of gambogic acid in B-cell Non-Hodgkin lymphoma and an inducer of histone H3 deacetylation

“…The overexpression of SRC-3 was reported to induce tumorigenesis and chemoresistance by modulating cancer-related signaling pathways, accelerating G1/S cycle transition, promoting the expression of anti-apoptotic proteins and inhibiting the expression of pro-apoptotic proteins (Ma et al, 2011;Oh et al, 2004). The interaction between SRC-3 and histone acetyltransferases (HATs) and histone deacetylases (HDACs) alter the acetylation of histones and influence the transcription of genes (Chang and Wu, 2012). Effective SRC-3 inhibitors have been proposed as a promising therapeutic strategy for these tumors (Tien and Xu, 2012).…”