The current study focused on
galectins (-1, -3, -4, -7, and -8) and deliberately performed immunohistochemical fingerprinting to explore their complexity in a context of experimental renal
carcinogenesis. The
diethylstilbestrol (DES)-induced renal
tumors in male Syrian hamster kidney (SHKT) represent a unique animal model for the study of
estrogen-dependent renal
malignancies. Kidney sections of DES-treated hamsters (3 days to 11 months of DES exposure) were analyzed by immunohistochemistry using a panel of non-crossreactive
antibodies raised against galectins-1, -3, -4, -7, and -8. Levels of expression were quantitatively determined by using computer-assisted microscopy on immunostained tissue sections. Except for
galectin-4, all above mentioned
galectins were expressed in kidney
tumors. Small clusters of galectin-1-positive, most likely preneoplastic cells at the corticomedullary junction were already evident 1 week after DES administration.
Galectin-1 and -3 expression was apparently associated with the first steps of the neoplastic transformation, because small tumorous buds were found to be positive after 1 month of treatment. In contrast, galectins-7 and -8 were detected in large
tumors and medium-sized
tumors, respectively, thereby indicating an involvement in later stages of DES-induced SHKT. Galectins-1, -3, -7, and -8 were also detected by immunofluorescence staining in the HKT-1097 cell line established from SHKT, thus illustrating the stability of
galectin expression in
tumor cells. Our data document the presence and differential regulation of
galectins in the course of renal
tumorigenesis in the model of DES-induced SHKT.