The role of AIB1 in breast cancer (Review)

  • Authors:
    • Alan K. Chang
    • Huijian Wu
  • View Affiliations

  • Published online on: July 16, 2012     https://doi.org/10.3892/ol.2012.803
  • Pages: 588-594
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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.
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October 2012
Volume 4 Issue 4

Print ISSN: 1792-1074
Online ISSN:1792-1082

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Spandidos Publications style
Chang AK and Chang AK: The role of AIB1 in breast cancer (Review). Oncol Lett 4: 588-594, 2012
APA
Chang, A.K., & Chang, A.K. (2012). The role of AIB1 in breast cancer (Review). Oncology Letters, 4, 588-594. https://doi.org/10.3892/ol.2012.803
MLA
Chang, A. K., Wu, H."The role of AIB1 in breast cancer (Review)". Oncology Letters 4.4 (2012): 588-594.
Chicago
Chang, A. K., Wu, H."The role of AIB1 in breast cancer (Review)". Oncology Letters 4, no. 4 (2012): 588-594. https://doi.org/10.3892/ol.2012.803