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Effects of DNA Methylation on Galectin-3 Expression in Pituitary Tumors

¹ Department of Pathology, Mayo Clinic College of Medicine, Rochester, Minnesota; ² Department of Pathology, St. Michael's Hospital, Toronto, Canada; and ³ Department of Pathology and Tumor Progression and Metastasis Program, Karmanos Cancer Institute, Wayne State University School of Medicine, Detroit, Michigan

Requests for reprints: Ricardo V. Lloyd, Department of Pathology and Laboratory Medicine, Mayo Clinic College of Medicine, Rochester, MN 55905. Phone: 507-284-4022; Fax: 507-284-1875; E-mail: lloyd.ricardo{at}mayo.edu.

Galectin-3 (Gal-3), a ß-galactoside-binding protein is expressed in a specific cell–type manner in pituitary tumors. Here we questioned the mechanism of Gal-3 expression in pituitary tumors, by using methylation-specific PCR and DNA sequence analyses to analyze the methylation status of the promoter region of the LGALS3 gene. DNA analysis of a human pituitary tumor, breast carcinoma cell lines, and thyroid carcinoma cell lines showed that in cells expressing Gal-3 protein, the LGALS3 gene was unmethylated, whereas in Gal-3 null cells, the promoter of the LGALS3 gene was methylated. Treatment of cells with 30 µmol/L 5-aza-2'-deoxycytidine induced Gal-3 mRNA and protein expression. Among pituitary tumors, 30% (7/23), mainly in follicle-stimulating hormone/luteinizing hormone–producing (38%) and null cell (57%) adenomas, the promoter of the LGALS3 was found to be methylated and silenced, although prolactin- and adrenocorticotropic hormone–producing tumors, which were unmethylated, expressed the Gal-3 protein. These results show for the first time that Gal-3 expression is regulated in part by promoter methylation in pituitary as well as in other tumors. Because it is functionally involved in cancer progression and metastasis, Gal-3 may serve as a possible therapeutic target in the treatment of pituitary tumors.

Key Words: Galectin-3 • methylation • pituitary tumors • PCR • cell culture

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