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Originally published online as doi:10.2353/ajpath.2009.080816 on March 12, 2009

Published online before print March 12, 2009
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(American Journal of Pathology. 2009;174:1515-1523.)
© 2009 American Society for Investigative Pathology
DOI: 10.2353/ajpath.2009.080816

Regulation of Prostate Cancer Progression by Galectin-3

Yi Wang*, Pratima Nangia-Makker*, Larry Tait{dagger}, Vitaly Balan*, Victor Hogan*, Kenneth J. Pienta{ddagger}§ and Avraham Raz*

From the Tumor Progression and Metastasis* and Breast Cancer Program,{dagger} Karmanos Cancer Institute, School of Medicine, Wayne State University, Detroit; and the Departments of Internal Medicine{ddagger} and Urology,§ University of Michigan, Ann Arbor, Michigan

Galectin-3, a β-galactoside-binding protein, has been implicated in a variety of biological functions including cell proliferation, apoptosis, angiogenesis, tumor progression, and metastasis. The present study was undertaken to understand the role of galectin-3 in the progression of prostate cancer. Immunohistochemical analysis of galectin-3 expression revealed that galectin-3 was cleaved during the progression of prostate cancer. Galectin-3 knockdown by small interfering RNA (siRNA) was associated with reduced cell migration, invasion, cell proliferation, anchorage-independent colony formation, and tumor growth in the prostates of nude mice. Galectin-3 knockdown in human prostate cancer PC3 cells led to cell-cycle arrest at G1 phase, up-regulation of nuclear p21, and hypophosphorylation of the retinoblastoma tumor suppressor protein (pRb), with no effect on cyclin D1, cyclin E, cyclin-dependent kinases (CDK2 and CDK4), and p27 protein expression levels. The data obtained here implicate galectin-3 in prostate cancer progression and suggest that galectin-3 may serve as both a diagnostic marker and therapeutic target for future disease treatments.


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