Research Overview
Interactions between cells, and between cells and the extracellular matrix (ECM) are pivotal for proper cellular function. It is now well established that protein-carbohydrate interactions play significant roles in modulating cell-cell and cell-ECM interactions, which, in turn, mediate various biological processes such as cell activation, growth regulation, cancer metastasis, and apoptosis. Thus, the identification of carbohydrate-binding proteins (lectins) and their partners (carbohydrate ligands), and the detailed understanding of the molecular mechanisms and downstream effects of these protein-carbohydrate interactions are subjects of current intense research. Galectins, a family of beta-galactoside-binding proteins, are differentially expressed during development and various stages of cancer. Our research is focused in basic and translational research of galectins. We have demonstrated that the expression of galectin-3 in prostate cancer is regulated by DNA methylation. Based on the measurement of the methylated DNA, a non-invasive method for early detection of prostate cancer in urine is being developed. Moreover, natural carbohydrate inhibitors of lectins and lectin-conjugates such as lectin-nanoparticle conjugates are being employed for the purpose of cancer diagnosis, prevention and drug delivery.
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Research DescriptionResearch Areas: Biochemistry, Glycobiology
Research Specialties: Protein-carbohydrate-interactions, basic and translational research of galectins and other lectins, epigenetics in normal functions and tumor development, diagnosis and prevention of cancers.
Research Interests: Structure, function, and
regulation of galectins. My research interest has been in the area of basic and translational
research of the carbohydrate-binding proteins (called lectins). Particularly, I
am interested in structure, function and regulation of galectins (a family of
beta-galactoside-binding lectins) and their interactions with the carbohydrates
that mediate cell-cell and cell-extracellular matrix (ECM) interactions during
normal and cancer development such as prostate
and breast cancers. The prostate cancer cells differentially express several
members of galectins, which alter normal cell-cell and cell-ECM interactions
during cancer development. We have discovered a novel isoform of galectin-8
that may be relevant to prostate cancer cell proliferation. Further, we have
demonstrated cytosine methylation in galectin promoter in cancerous prostate,
which may account for the differential expression of galectins during cancer
development. Differential expression of galectin repertoire and identification
of cytosine methylation of galectin gene promoters in normal and prostate
tissues are now being employed to develop sensitive tools for early diagnosis
of prostate cancer in biological fluids such as serum and urine. In another
project, natural carbohydrate inhibitors of galectin are being employed to
prevent breast cancer metastasis.
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Representative Publications
Ahmed, H., Cappello, F.,
Rodolico, V., and Vasta, G.R. 2009. Evidence
of heavy methylation in the galectin-3 promoter in early stages of prostate
adenocarcinoma: Development and validation of a methylated marker for early
diagnosis of prostate cancer. Translational Oncology (Accepted)
Ahmed, H., Du, S.J.,
and Vasta, G.R. 2008. Knockdown of a galectin-1-like protein in zebrafish (Danio rerio) causes defects in skeletal
muscle development. Glycoconjugate J. Sep 2. [Epub ahead of print]
Ahmed, H., Banerjee, P.B., and Vasta, G.R. 2007. Differential expression of galectins in normal, benign and
malignant prostate epithelial cells: Silencing of galectin-3 expression in
prostate cancer by its promoter methylation. Biochem. Biophys. Res. Commun.
358, 241-246.
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