The mechanisms leading to rapid invasive growth of malignant gliomas are po
orly understood. Expression of the hyaluronic acid (HA) receptor CD44 and a
dhesion to HA are involved in invasive properties. Our previous studies hav
e shown that malignant glioma cells are able to adhere to extracellular HA.
Here we investigated expression of the hyaluronic acid receptor CD44 prote
in in five human (T98G, A172, U87MG, 86HG39, 85HG66) and two rat (C6, 9L) g
lioma cell lines. Influence of anti-CD44 antibody and hyaluronidase-preincu
bation on the HA-binding was determined using HA/BSA (bovine serum albumin)
-coated culture plates. While all gliomas were highly positive for CD44 wit
h no differences in the number of positive staining cells, median fluoresce
nce intensity decreased as follows: C6>T98G>9L>85HG66> 86HG39>A172> U87MG.
Using HA/BSA coated culture plates the relative levels of specific adhesion
to HA were determined as T98G>A172>9L>86HG39>U87MG>85HG66. C6 cells failed
to bind HA specifically. Incubation with anti-human-CD44 MAb significantly
decreased HA-adhesion of T98G, A172, 85HG66 and U87MG human glioma cells.
However the binding capacity was completely blocked only in 85HG66 cells. T
he three other cell lines kept a specific HA-adhesion after saturation of t
he receptor. Hyaluronidase pretreatment markedly enhanced HA-adhesion of C6
and 9L rat glioma cells. These results suggest that (i) HA-adhesion of mal
ignant glioma cells is mainly, but not only, mediated by CD44, (ii) express
ion of CD44 does not correspond with adhesion capacity and (iii) cell-bound
glycosaminoglycans may influence glioma cell adhesion to extracellular HA.