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Breast Cancer–Amplified Sequence 3, a Target of Metastasis-Associated Protein 1, Contributes to Tamoxifen Resistance in Premenopausal Patients with Breast Cancer
Anupama E. Gururaj, Caroline Holm, Göran Landberg and Rakesh Kumar
volume 5 | issue 13
1 july 2006Pages: 1407 - 1410
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Lysine acetylation occurs in many protein targets, including core histones, transcription factors, and other proteins. Metastasis-associated protein 1 (MTA1) is implicated in the progression and metastasis of various epithelial tumors. Because MTA1 functions as a transcriptional coregulator, much of its role in cancer promoting processes are likely to involve its ability to regulate the transcription of downstream target genes that encode effector proteins. We recently showed that MTA1 could be posttranslationally modified by acetylation, which modulates its function as a coregulator molecule. We also defined a chromatin target of MTA1, namely, breast cancer–amplified sequence 3 (BCAS3), in the context of which MTA1 behaves as a transcriptional coactivator in breast cancer cells. Because the phenotypic effect of BCAS3 overexpression in tumors has not been defined, we investigated the consequence of increased expression of BCAS3 in human breast tumors. Here, we report that BCAS3 overexpression in hormone receptor–positive premenopausal breast cancer seemed to be associated with impaired responses to tamoxifen.. Our findings have implications for endocrine therapy.
We now provide open access to journal articles published online for one year or more. This article may be downloaded at the following link:
Download PDF If the document does not open, please right-click on the link (control-click on a Macintosh) and select the option to save the file to disk.