Role of AIB1 for Tamoxifen Resistance in Estrogen Receptor-Positive Breast Cancer Cells

Su, Qingbo; Hu, Sanyuan; Gao, Haidong; Ma, Rong; Yang, Qifeng; Pan, Zhengxia; Wang, Tiantian; Li, Feng

doi:10.1159/000159267

Cited by 44 publications

(43 citation statements)

References 101 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…AIB1 is the only SRC family member that is strongly amplified and overexpressed in human breast cancer and is implicated in tamoxifen resistance (11)(12)(13)(14)(15). Depletion of AIB1 in MCF-7 cells reduces estrogen-mediated cell growth, inhibition of apoptosis, colony formation in soft agar, and tumor growth in nude mice (45).…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

ATBF1 Inhibits Estrogen Receptor (ER) Function by Selectively Competing with AIB1 for Binding to the ER in ER-positive Breast Cancer Cells*

Dong

Sun

Guo

et al. 2010

Journal of Biological Chemistry

View full text Add to dashboard Cite

Loss of the q22 band of chromosome 16 is a frequent genetic event in breast cancer, and the candidate tumor suppressor gene, ATBF1, has been implicated in breast cancer by genomic deletion, transcriptional down-regulation, and association with better prognostic parameters. In addition, estrogen receptor (ER)-positive breast cancer expresses a higher level of ATBF1, suggesting a role of ATBF1 in ER-positive breast cancer. In this study, we examined whether and how ATBF1 affects the ER function in breast cancer cells. We found that ATBF1 inhibited ER-mediated gene transcription, cell growth, and proliferation in ER-positive breast cancer cells. In vitro and in vivo immunoprecipitation experiments revealed that ATBF1 interacted physically with the ER and that multiple domains in both ATBF1 and ER proteins mediated the interaction. Furthermore, we demonstrated that ATBF1 inhibited ER function by selectively competing with the steroid receptor coactivator AIB1 but not GRIP1 or SRC1 for binding to the ER. These findings not only support the concept that ATBF1 plays a tumor-suppressive role in breast cancer, they also provide a mechanism for how ATBF1 functions as a tumor suppressor in breast cancer.

show abstract

Section: Discussionmentioning

confidence: 99%

“…The significance of SRCs in breast cancer has been an area of extensive study. AIB1 is the only SRC family member that is strongly amplified and overexpressed in human breast cancer and implicated in tamoxifen resistance (11)(12)(13)(14)(15). AIB1 promotes tumorigenesis and is essential for HER2-driven oncogenesis in mice (16 -18).…”

mentioning

confidence: 99%

ATBF1 Inhibits Estrogen Receptor (ER) Function by Selectively Competing with AIB1 for Binding to the ER in ER-positive Breast Cancer Cells*

Dong

Sun

Guo

et al. 2010

Journal of Biological Chemistry

View full text Add to dashboard Cite

show abstract

“…In addition, variation in cofactor expression levels during tumorigenesis may contribute to resistance to AEs (Osborne et al . 2003, Su et al . 2008).…”

Section: Impact Of Ae-induced Erα Conformation On Cofactor Recruitmenmentioning

confidence: 99%

Antiestrogens: structure-activity relationships and use in breast cancer treatment

Traboulsi

Ezzy

Gleason

et al. 2017

Journal of Molecular Endocrinology

View full text Add to dashboard Cite

About 70% of breast tumors express estrogen receptor alpha (ERα), which mediates the proliferative effects of estrogens on breast epithelial cells, and are candidates for treatment with antiestrogens, steroidal or non-steroidal molecules designed to compete with estrogens and antagonize ERs. The variable patterns of activity of antiestrogens (AEs) in estrogen target tissues and the lack of systematic cross-resistance between different types of molecules have provided evidence for different mechanisms of action. AEs are typically classified as selective estrogen receptor modulators (SERMs), which display tissue-specific partial agonist activity (e.g. tamoxifen and raloxifene), or as pure AEs (e.g. fulvestrant), which enhance ERα post-translational modification by ubiquitin-like molecules and accelerate its proteasomal degradation. Characterization of second- and third-generation AEs, however, suggests the induction of diverse ERα structural conformations, resulting in variable degrees of receptor downregulation and different patterns of systemic properties in animal models and in the clinic.

show abstract

“…In fact, SRC3 was originally identified as amplified-in-breast cancer 1 (AIB1), which was found overexpressed in breast and ovarian cancers (20). Up-regulation of the SRC3 activity promotes breast cancer growth, invasiveness, and resistance to antiestrogen (21,22). In parallel, SRC3 is found to be overexpressed in prostate cancer cells (23) and is correlated with human prostate cancer seminal vesicle invasion and lymph node metastasis (24).…”

Section: The Androgen Receptor (Ar)mentioning

confidence: 99%

Identification of SRC3/AIB1 as a Preferred Coactivator for Hormone-activated Androgen Receptor

Zhou

Suino-Powell

et al. 2010

Journal of Biological Chemistry

View full text Add to dashboard Cite

Transcription activation by androgen receptor (AR), which depends on recruitment of coactivators, is required for the initiation and progression of prostate cancer, yet the mechanisms of how hormone-activated AR interacts with coactivators remain unclear. This is because AR, unlike any other nuclear receptor, prefers its own N-terminal FXXLF motif to the canonical LXXLL motifs of coactivators. Through biochemical and crystallographic studies, we identify that steroid receptor coactivator-3 (SRC3) (also named as amplified in breast cancer-1 or AIB1) interacts strongly with AR via synergistic binding of its first and third LXXLL motifs. Mutagenesis and functional studies confirm that SRC3 is a preferred coactivator for hormoneactivated AR. Importantly, AR mutations found in prostate cancer patients correlate with their binding potency to SRC3, corroborating with the emerging role of SRC3 as a prostate cancer oncogene. These results provide a molecular mechanism for the selective utilization of SRC3 by hormone-activated AR, and they link the functional relationship between AR and SRC3 to the development and growth of prostate cancer.

show abstract

Role of AIB1 for Tamoxifen Resistance in Estrogen Receptor-Positive Breast Cancer Cells

Cited by 44 publications

References 101 publications

ATBF1 Inhibits Estrogen Receptor (ER) Function by Selectively Competing with AIB1 for Binding to the ER in ER-positive Breast Cancer Cells*

ATBF1 Inhibits Estrogen Receptor (ER) Function by Selectively Competing with AIB1 for Binding to the ER in ER-positive Breast Cancer Cells*

Antiestrogens: structure-activity relationships and use in breast cancer treatment

Identification of SRC3/AIB1 as a Preferred Coactivator for Hormone-activated Androgen Receptor

Contact Info

Product

Resources

About