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An N-terminal splice variant of human Stat5a that interacts with different transcription factors is the dominant form expressed in invasive ductal carcinoma

Authors
  • Tan, Dunyong
  • Chen, KuanHui E.
  • Deng, Changhui
  • Tang, Peizhi
  • Huang, Jianjun
  • Mansour, Trina
  • Luben, Richard A.
  • Walker, Ameae M.1, 2, 3, 2, 4, 5, 6, 5
  • 1 Division of Biomedical Sciences
  • 2 University of California, Riverside
  • 3 Department of Biochemistry
  • 4 College of Medicine/Institute of Medical Sciences
  • 5 Jishou University
  • 6 People’s Hospital of Xiangxi Autonomous Region
Type
Published Article
Journal
Cancer Letters
Publisher
Elsevier
Publication Date
Jan 01, 2014
Accepted Date
Dec 20, 2013
Volume
346
Issue
1
Pages
148–157
Identifiers
DOI: 10.1016/j.canlet.2013.12.030
Source
Elsevier
Keywords
License
Unknown

Abstract

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 Δ5 Stat5a interacts with activating protein 1–2 and specificity protein 1. Prolactin also oppositely regulates interaction of the two Stat5a forms with β-catenin. We propose that a change in splicing leading to upregulation of this new isoform is a pathogenic aspect of invasive ductal carcinoma.

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