Lectin histochemistry of astrocytic tumors and in vitro characterization of lectin-induced modifications on the proliferation of the SW1088, U373 and U87 human astrocytic cell lines.

The role of lectins as biosignalling molecules or as markers of human astrocytic tumors remains relatively unexplored. The aim of the present work is to investigate (1) whether or not human astrocytic tumors express specific glycans, evidenced experimentally by means of lectin histochemistry, and (2) whether, in turn, these lectins can significantly modulate astrocytic tumor cell proliferation. Using a cell image processor, we therefore began by quantitatively measuring the histochemical binding pattern of 5 lectins (WGA, PNA, PHA-L, GSA-IA4 and Con A) in 5 astrocytomas, 5 anaplastic astrocytomas and 5 glioblastomas. Secondly, we measured the influence of these 5 lectins on the proliferation of 3 astrocytic tumor cell lines (SW1088, U373 and U87) growing in vitro as monolayers. Cell proliferation was assessed by means of the colorimetric MTT assay. The histochemical lectin staining markedly varied intra- and inter-group. However, some constant results were obtained. Indeed, the staining increased markedly from GSA-IA4 and PHA-L through WGA and PNA to ConA in the three histopathological groups. The assessment of cell proliferation demonstrated that WGA, Con A and PHA-L very significantly decreased proliferation in the 3 astrocytic cell lines in a dose-dependent manner. Astrocytic tumor cells in the confluent growth phase were less sensitive to the WGA, Con A and PHA-L lectin-induced effects than cells in the log growth phase. The GSA-IA4 and PNA lectins had globally very weak effects on the proliferation of the astrocytic tumor cell lines. Increasing the fetal calf serum from 1% to 10% in the culture media significantly antagonized the WGA-, Con A- and PHA-L-induced cell proliferation decrease in the 3 astrocytic cell lines. In conclusion, the present data strongly suggest that some lectins (including WGA, Con A and PHA-L) significantly influence the proliferation of astrocytic tumor cells.