The impact of dexamethasone on cellular stress responses caused by mild serum deprivation in androgen-insensitive prostate cancer cells.

Dexamethasone (DEX), a glucocorticoid receptor agonist, is widely used for prostate cancer therapies, although its exact impact on androgen-independent prostate cancer cells remains unclear. As solid cancers are typically characterized by nutrient-deprived conditions in the tumor microenvironment (TME), the present study examines the effect of DEX on stress responses in DU-145 and PC3 cells caused by mild serum deficiency. It was found that DEX limited the ability of prostate cancer cells to divide and deepened the G0 / G1 cell cycle arrest induced by serum deprivation; it also reduced adhesion by DU-145 and PC3 cells to extracellular matrix proteins, but did not increase migration. However, it improved the survival of androgen-insensitive prostate cancer cells under conditions of mild serum deprivation by preventing apoptosis, reprogramming the glucose and lipid metabolism and restoring the inflammatory balance. We postulate that dexamethasone has a cytostatic rather than cytotoxic effect on androgen-independent prostate cancer cells and that it directs prostate cancer cells to a resting state. Treatment also carries a risk of minimal residual disease (MRD).