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Overexpression of the Protein Tyrosine Phosphatase PRL-2 Correlates with Breast Tumor Formation and Progression Serge Hardy, Nau Nau Wong, William J. Muller, Morag Park, and Michel L. Tremblay Authors' Affiliation: The Goodman Cancer Center and Department of Biochemistry, McGill University, Montreal, Quebec, Canada Corresponding Author:Michel L. Tremblay, The Goodman Cancer Center, McGill University, 1160 Des Pins Avenue West, Cancer Pavilion, Room 617, Montreal, Quebec, Canada H3A 1A3. Phone: 514-398-7290; Fax: 514-398-6769; E-mail: michel.tremblay{at}mcgill.ca. Abstract The PRL-1, PRL-2, and PRL-3 phosphatases are prenylated protein tyrosine phosphatases with oncogenic activity that are proposed to drive tumor metastasis. We found that PRL-2 mRNA is elevated in primary breast tumors relative to matched normal tissue, and also dramatically elevated in metastatic lymph nodes compared with primary tumors. PRL-2 knockdown in metastatic MDA-MB-231 breast cancer cells decreased anchorage-independent growth and cell migration, suggesting that the malignant phenotype of these cells is mediated at least in part through PRL-2 signaling. In different mouse mammary tumor–derived cell lines overexpressing PRL-2, we confirmed its role in anchorage-independent growth and cell migration. Furthermore, injection of PRL-2–overexpressing cells into the mouse mammary fat pad promoted extracellular signal-regulated kinase 1/2 activation and tumor formation. MMTV–PRL-2 transgenic mice engineered to overexpress the enzyme in mammary tissue did not exhibit spontaneous tumorigenesis, but they exhibited an accelerated development of mammary tumors initiated by introduction of an MMTV-ErbB2 transgene. Together, our results argue that PRL-2 plays a role in breast cancer progression. Cancer Res; 70(21); 8959–67. ©2010 AACR. Footnotes Note: Supplementary data for this article are available at Cancer Research Online (http://cancerres.aacrjournals.org/). Received June 10, 2010. Revision received September 9, 2010. Accepted September 10, 2010. ©2010 American Association for Cancer Research.
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Twitter What's this? « Previous | Next Article »Table of Contents This Article Published OnlineFirst September 14, 2010; doi: 10.1158/0008-5472.CAN-10-2041 Cancer Res November 1, 2010 70; 8959 » Abstract Full Text Full Text (PDF) Supplementary Data All Versions of this Article: 0008-5472.CAN-10-2041v1 0008-5472.CAN-10-2041v2 70/21/8959 most recent Classifications Tumor and Stem Cell Biology Services Email this article to a colleague Alert me when this article is cited Alert me if a correction is posted Similar articles in this journal Similar articles in PubMed Download to citation manager 
Citing Articles Load citing article information Citing articles via Scopus Google Scholar Articles by Hardy, S. Articles by Tremblay, M. L. PubMed PubMed citation Articles by Hardy, S. Articles by Tremblay, M. L. Social Bookmarking CiteULike Complore Connotea Del.icio.us Digg Facebook Reddit Technorati Twitter What's this? :: AACR Publications Home :: 
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