We have shown that glucocorticoids reversibly change the growth control of rat C6 glioma cells from a transformed to a normal pattern. Here we report that the glucocorticoid hormone hydrocortisone (Hy) modulates structure and function of cell surface and cytoskeleton. The hormone is shown to cause: (a) increased flattening and adhesion to solid substrates and to fibrin layers, (b) inhibition of the cell shape change triggered by catecholamines and cAMP, (c) extensive fibronectin deposition on normally fibronectinless cells' surface, and (d) microtubule rearrangement. Comparison of Hy-hypersensitive and Hy-resistant variants showed that microtubule rearrangements correlate with the growth control change induced by Hy, whereas fibronectin deposition does not.

We undertook a comparative study of the effects of the hormone hydrocortisone (Hy) on C6 glioma cells grown in monolayer and in suspension in cultures. We found Hy reversibly renders C6 cells anchorage- and serum-dependent for their growth. In monolayer cultures, Hy was found to inhibit cell cycle traversing exclusively at G1 phase. In agarose suspension, Hy was found to block colony development. Hy-resistant variants were selected and isolated in agarose suspension. Examination of these variants showed that cells selected for Hy-resistance in suspension can be Hy sensitive when anchored to a solid substrate. We conclude that resistance to Hy in suspension and resistance to it in monolayer culture are two independent phenotypes.