TY - JOUR
T1 - Regulation of prostate cancer progression by galectin-3
AU - Wang, Yi
AU - Nangia-Makker, Pratima
AU - Tait, Larry
AU - Balan, Vitaly
AU - Hogan, Victor
AU - Pienta, Kenneth J.
AU - Raz, Avraham
N1 - Funding Information:
Supported by the National Institutes of Health (grants R37CA46120-19 to A.R. and P50 CA69568 to K.P. ), the Karmanos Cancer Institute (strategic research grant to A.R. and P.N.-M.), and the American Cancer Society (clinical research professor to K.J.P.).
PY - 2009/4
Y1 - 2009/4
N2 - 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 ofgalectin-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 hypo- hosphorylation 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.
AB - 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 ofgalectin-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 hypo- hosphorylation 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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U2 - 10.2353/ajpath.2009.080816
DO - 10.2353/ajpath.2009.080816
M3 - Article
C2 - 19286570
AN - SCOPUS:65349183478
SN - 0002-9440
VL - 174
SP - 1515
EP - 1523
JO - American Journal of Pathology
JF - American Journal of Pathology
IS - 4
ER -