Journal
CANCER LETTERS
Volume 346, Issue 1, Pages 148-157Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.canlet.2013.12.030
Keywords
Breast cancer; Invasive ductal carcinoma; Stat5a; Splice variant; Interaction with other signaling/; transcription factors
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Funding
- United States Public Health Service [DK61005]
- California Breast Cancer Research Program [171B-0053]
- National Natural Science Foundation of China [81172497]
- Jishou University [jsdxkyzz101010]
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We have identified a new variant of human Stat5a, found at higher ratios to full-length Stat5a in invasive ductal carcinoma versus contiguous normal tissue. The variant, missing exon 5, inhibits p21 and Bax production and increases cell number. After prolactin stimulation, only full-length Stat5a interacts with the vitamin D and retinoid X receptors, whereas only Delta 5 Stat5a interacts with activating protein 1-2 and specificity protein 1. Prolactin also oppositely regulates interaction of the two Stat5a forms with beta-catenin. We propose that a change in splicing leading to upregulation of this new isoform is a pathogenic aspect of invasive ductal carcinoma. (C) 2014 The Authors. Published by Elsevier Ltd. All rights reserved.
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