Involvement of decreased galectin-3 expression in the pathogenesis and progression of prostate cancer

Axel S. Merseburger, Mario W. Kramer, Jörg Hennenlotter, Perikles Simon, Judith Knapp, Jörg T. Hartmann, Arnulf Stenzl, Jürgen Serth, Markus A. Kuczyk*

*Corresponding author for this work
42 Citations (Scopus)


BACKGROUND. Altered expression or loss of function of Galectin-3 (Gal-3) was suggested to be involved in the pathogenesis and progression of various human cancer entities. The aim of the present study is to determine the expression of Gal-3 in prostate tissue emerging from a benign to a malignant, in the beginning hormone-sensitive and finally hormone-refractory status to further elucidate the role of this carbohydrate-binding protein for the pathogenesis and/or progression of malignant prostatic disease. MATERIALS AND METHODS. Five hundred and eighty three tissue samples from malignant, tumor adjacent benign, and histologically benign intra-prostatic areas, retrieved out of 25 whole mounted prostate cancer (CaP) specimens and additional 95 samples of hormone-refractory CaP, were processed to tissue microarrays. Immunohistochemical Gal-3 expression was correlated with clinicopathological parameters among the different tissue entities. RESULTS. Gal-3 expression was significantly decreased in the hormone-sensitive CaP specimens when compared with the respective benign tissue either localized far distant from the malignant lesion (P < 0.0001, Wilcoxon test) or directly neighboring the primary tumor (P < 0.0001). The staining reaction in the benign tissue areas directly neighboring the primary cancerous lesions differed significantly from the benign glands localized distant from the primary tumors (P < 0.001). A statistically highly significant, almost complete loss of Gal-3 was observed in the hormone-refractory when compared with the hormone-sensitive tumors (P < 0.0001; mean staining score: 27.7% vs. 8.5%). CONCLUSIONS. The present investigation clearly indicates decreased expression of Gal-3 to be substantially involved in the pathogenesis and further progression of CaP from benign prostate glands to a finally hormone-refractory malignant disease.

Original languageEnglish
Issue number1
Pages (from-to)72-77
Number of pages6
Publication statusPublished - 01.01.2008

Research Areas and Centers

  • Research Area: Luebeck Integrated Oncology Network (LION)


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