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Cancer Research 68, 467, January 15, 2008. doi: 10.1158/0008-5472.CAN-07-0782
© 2008 American Association for Cancer Research

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Cell, Tumor, and Stem Cell Biology

Cyclooxygenase-2 Expression during Immortalization and Breast Cancer Progression

Xiangshan Zhao1, Monica Goswami1,3, Nidhi Pokhriyal1, Hui Ma1, Hongyan Du4, Jun Yao6, Thomas A. Victor3, Kornelia Polyak6, Charles D. Sturgis3, Hamid Band2,5 and Vimla Band1,5

Divisions of 1 Cancer Biology and 2 Molecular Oncology, Department of Medicine, 3 Department of Pathology, and 4 Center for Outcome Research and Education, Evanston Northwestern Healthcare Research Institute and Feinberg School of Medicine; 5 Department of Biochemistry, Molecular Biology and Cell Biology, Northwestern University, Evanston, Illinois; and 6 Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts

Requests for reprints: Vimla Band, Department of Genetics, Cell Biology & Anatomy, University of Nebraska Medical Center, DRC 6th Floor, 985805 Nebraska Medical Center, Omaha, NE 68198-5805. Phone: 402-559-8565; Fax: 402-559-7328; E-mail: vband{at}unmc.edu.

Identification of molecular aberrations in premalignant human mammary epithelial cells (hMEC), the precursors for breast cancers, is a central goal in breast cancer biology. Recent studies implicated expression of cyclooxygenase 2 (COX-2) as a marker to identify precursor cells for breast cancer. In this study, we analyzed COX-2 expression in preselection and postselection hMEC cells and observed similar COX-2 levels in both cells. Interestingly, immortalization of postselection cells using various methods leads to a dramatic decrease in COX-2 expression. Similar to immortal cells, the majority of breast cancer cell lines expressed low levels of COX-2 protein. Finally, analyses of COX-2 expression in a series of specimens from reduction mammoplasty, adenosis, ductal carcinoma in situ, and infiltrating ductal carcinoma showed down-regulation of COX-2 expression during tumor progression. Importantly, down-regulation of COX-2 using small interfering RNA in cells showed no effect on cell proliferation, anchorage-independent growth, migration, or invasion. These results show that (a) COX-2 overexpression does not seem to predict a breast cancer precursor cell and does not provide advantage for the cell to be transformed; (b) inhibition of COX-2 does not affect hMEC growth and oncogenic behavior in the conditions analyzed; and (c) COX-2 expression is decreased in breast cancer cell lines and cancer specimens as compared with normal mammary epithelial cells. [Cancer Res 2008;68(2):467–75]




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Correction: COX-2 Expression Decreases in Breast Cancer Progression
Cancer Res., March 1, 2008; 68(5): 1609 - 1609.
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Copyright © 2008 by the American Association for Cancer Research.