Wnt/β‐Catenin‐Responsive Cells in Prostatic Development and Regeneration. (29th July 2015)

• Record Type: Journal Article
• Authors: Lee, Suk Hyung; Johnson, Daniel T.; Luong, Richard; Yu, Eun Jeong; Cunha, Gerald R.; Nusse, Roel; Sun, Zijie
• Is Part Of: Stem cells. Volume 33:Number 11(2015:Nov.)
• Page Start: 3356
• Page End: 3367
• Publication Date: 2015-07-29
• Subjects: Cloning -- Periodicals; Clone cells -- Periodicals; Stem cells -- Periodicals; Cell Differentiation -- Periodicals; Cell Division -- Periodicals; Clone Cells -- Periodicals; Hematopoietic Stem Cells -- Periodicals; Stem Cells -- Periodicals; 571.84
• DOI: 10.1002/stem.2096
• Languages: English
• ISSNs: 1066-5099

Abstract

<abstract abstract-type="main"> <title>A<sc>bstract</sc></title> <p>The precise role of Wnt/β‐catenin signaling during prostatic development and tumorigenesis is unclear. <italic>Axin2</italic> is a direct transcriptional target of β‐catenin. Recent studies have shown that <italic>Axin2</italic>‐expressing cells have stem/progenitor cell properties in a variety of mouse tissues. Here, we genetically labeled <italic>Axin2</italic>‐expressing cells at various time points and tracked their cellular behavior at different developmental and mature stages. We found that prostatic <italic>Axin2</italic>‐expressing cells mainly express luminal epithelial cell markers and are able to expand luminal cell lineages during prostatic development and maturation. They can also survive androgen withdrawal and regenerate prostatic luminal epithelial cells following androgen replacement. Deletion of β‐catenin or expression of stabilized β‐catenin in these <italic>Axin2</italic>‐expressing cells results in abnormal development or oncogenic transformation, respectively. Our study uncovers a critical role of Wnt/β‐catenin‐responsive cells in prostatic development and regeneration, and that dysregulation of Wnt/β‐catenin signaling in these cells contributes to prostatic developmental defects and tumorigenesis. S<sc>tem</sc> C<sc>ells</sc><italic>2015;33:3356–3367</italic></p> </abstract>