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This version published online on July 8, 2004
Molecular Endocrinology, doi:10.1210/me.2004-0163
A more recent version of this article appeared on October 1, 2004
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Submitted on April 19, 2004
Accepted on July 1, 2004

Re-expression of p8 Contributes to Tumorigenic Properties of Pituitary Cells and Appears in a Subset of Prolactinomas in Transgenic Mice that Hypersecrete LH

Helai P Mohammad, Darcie D Seachrist, Christine C Quirk, and John H Nilson*

Department of Pharmacology, Case Western Reserve University, Cleveland, OH 44106

* To whom correspondence should be addressed. E-mail: jhn{at}wsu.edu.

Targeted overexpression of luteinizing hormone (LH) in transgenic mice causes hyperproliferation of Pit-1 positive pituitary cells and development of functional adenomas. To characterize gene expression changes associated with pituitary tumorigenesis, we performed microarray studies using Affymetrix GeneChips comparing expression profiles from pituitary tumors in LH-overexpressing mice to wild-type control pituitaries. We identified a number of candidate genes with altered expression in pituitary tumors. One of these, p8 (com1), encodes a native high mobility group (HMG) like transcription factor previously shown to be necessary for ras-mediated transformation of mouse embryonic fibroblasts and also implicated in breast cancer progression. Herein, we show that expression of p8, normally quiescent in adult pituitary, localizes to tumor foci containing lactotropes, suggesting a linkage with their transformation. To further establish the functional significance of p8 in pituitary tumorigenesis, we constructed several clonal cell lines with reduced expression of p8 from a parent GH3 somato-lacotrope cell line. These clonal derivates, along with the parent cell line, were tested for tumorigenicity by injection into athymic mice. When compared with wild-type GH3 with higher levels of p8, GH3 cells with reduced expression of p8 displayed attenuated tumor development or failed to develop tumors at all. Similar results were obtained with gonadotrope derived cell lines that displayed reduced expression of p8. Together, these data suggest that maintenance of the transformed phenotype of pituitary GH3 cells requires expression of p8 and that it may play a similar role when re-expressed in a subset of lactotropes that form prolactinomas in vivo.
Key words: LH • pituitary adenoma • transgenic mice • p8 • expression profiling




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